ncRNA_name	ncRNAID	ncRNA type	Subcellular location	Species	Diseases	Cell lines/Tissue	Techniques	Used reagents	target	Ferroptosis pathway/component	Regulation	Description	Title	Year	PMID
circRNA1615	-	circRNA	-	mouse	Myocardial Infarction	cardiomyocytes	Luciferase Reporter Experiments	erastin	miRNA152-3p/LRP6	GPX4	circRNA1615 inhibits ferroptosis	circRNA1615 inhibited ferroptosis in cardiomyocytes, and circRNA1615 could regulate the expression of LRP6 through sponge adsorption of miR-152-3p, prevent LRP6-mediated autophagy-related ferroptosis in cardiomyocytes, and finally control the pathological process of MI.	Effect and Mechanism of LRP6 on Cardiac Myocyte Ferroptosis in Myocardial Infarction	2021	34712388
circGFRA1	-	circRNA	-	H.sapiens	Breast Cancer	breast cancer tissues	Western blotting	-	miR-1228-AIFM2	GPX4	knockdown of circGFRA1 promotes ferroptosis	Combined with the confirmation that the decrease in the GSH/GSSG ratio results in the deactivation of GPX4, which in turn leads to more toxic lipid reactive oxygen species (ROS) accumulation and ferroptosis induction, we can deduce that knockdown of circGFRA1 promotes ferroptosis. In addition, it has been proven that the two pathways mentioned above act in parallel with each other.	CircGFRA1 facilitates the malignant progression of HER-2-positive breast cancer via acting as a sponge of miR-1228 and enhancing AIFM2 expression	2021	34668628
circDTL	-	circRNA	cytoplasm/Nuclear	H.sapiens	Non-Small Cell Lung Cancer	 lung epithelial cell line BEAS-2B and human NSCLC cell lines	CCK-8 assay	erastin	miR-1287-5p/GPX4	lipid ROS	silencing of circDTL induced ferroptosis 	This study found that circDTL was upregulated and acted as an oncogene during the progression of NSCLC. Interestingly, silencing of circDTL induced ferroptosis of NSCLC cells and further investigation showed that circDTL regulated ferroptosis via the miR-1287-5p/GPX4 axis. These findings underlined the importance of circRNAs in the process of ferroptosis and introduced circDTL as a regulator of ferroptosis in NSCLC.	CircDTL Functions as an Oncogene and Regulates Both Apoptosis and Ferroptosis in Non-small Cell Lung Cancer Cells	2021	34621297
circRHBG	-	circRNA	-	H.sapiens	Polycystic Ovary Syndrome	KGN and SVOG cells	CCK-8 assay	-	miR515-5p/SLC7A11	glutathione	circRHBG knockdown promotes ferroptosis	CircRNA high-throughput chips and qRT-PCR verified that circRHBG was significantly upregulated in granular cells of PCOS patients. Knockdown of circRHBG inhibits KGN and SVOG cell proliferation. Luciferase reporter assays and Ago2-RIP detection showed that circRHBG competes with SLC7A11 to bind to miR-515-5p. Subsequent experiments verified knockdown of circRHBG promotes ferroptosis in PCOS.	Involvement of ferroptosis in the granulosa cells proliferation of PCOS through the circRHBG/miR-515/SLC7A11 axis	2021	34532485
circFNDC3B	-	circRNA	-	H.sapiens	Oral Squamous Cell Carcinoma	CAL27 and SCC15 cell lines	CCK-8 assay	erastin	miR-520d-5p/SLC7A11	lipid ROS	circFNDC3B attenuated ferroptosis	Our data demonstrated that the silencing of circFNDC3B by shRNA inhibited GPX4 and SLC7A11 expression and enhanced ROS, iron, and Fe2+ levels in OSCC cells. CircFNDC3B knockdown reinforced erastin-induced inhibitory effect on OSCC cells. The depletion of circFNDC3B repressed cell proliferation and enhanced cell apoptosis of OSCC cells.	Circular RNA FNDC3B Protects Oral Squamous Cell Carcinoma Cells From Ferroptosis and Contributes to the Malignant Progression by Regulating miR-520d-5p/SLC7A11 Axis	2021	34434890
circ_0067934	-	circRNA	-	H.sapiens	Thyroid Cancer	FTC133 and TPC-1 cells	DCFH-DA staining	-	miR-545-3p/SLC7A11	lipid ROS	Circ_0067934 attenuated ferroptosis	The knockdown of circ_0067934 induced thyroid cancer cell apoptosis and repressed thyroid cancer cell proliferation in vitro and in vivo. Circ_0067934 upregulated the expression of the ferroptosis-negative regulator SLC7A11 by sponging and inhibiting miR-545-3p in thyroid cancer cells. The overexpression of SLC7A11 or the inhibitor of miR-545-3p reversed circ_0067934 silencing-regulated thyroid cancer cell proliferation. 	Circular RNA Circ_0067934 Attenuates Ferroptosis of Thyroid Cancer Cells by miR-545-3p/SLC7A11 Signaling	2021	34290668
circKIF4A	-	circRNA	-	H.sapiens	Thyroid Cancer	thyroid tissues and primary papillary thyroid cancer samples	-	-	miR-1231/GPX4	GPX4	circKIF4A facilitated the malignant progress	We explored circKIF4A and the result showed that it had high expression in papillary thyroid cancer. The functions of circKIF4A were explored by CCK-8, transwell, and mouse xenograft experiments. Knockdown of circKIF4A could suppress papillary thyroid cell growth and migration. In addition, RIP assays and dual luciferase vector reporter assays were further conducted. Our consequence showed circKIF4A facilitated the malignant progress of papillary thyroid tumor by sponging miR-1231 and upregulating GPX4 expression. In conclusion, our study proved that circKIF4A-miR-1231-GPX4 axis played a vital role in cancer proliferation and ferroptosis by competing endogenous RNAs.	Circular RNA circKIF4A facilitates the malignant progression and suppresses ferroptosis by sponging miR-1231 and upregulating GPX4 in papillary thyroid cancer	2021	34153004
circ0097009	-	circRNA	-	H.sapiens	Hepatocellular Cancer	LO2 and HCC cell lines HepG2, BEL-7402, and MHCC-97H	Glutathione	-	miR-1261/SLC7A11	GPX4	knockdown of circ0097009 promotes ferroptosis	Microarray analysis and qRT-PCR verified that circRNA, circ0097009, was significantly upregulated in HCC tissues and cell lines. Knockdown of circ0097009 inhibited the proliferation and invasion of HCC cells. Luciferase reporter assays showed that circ0097009 and SLC7A11 directly bound to miR-1261. Subsequent experiments showed that circ0097009 and SLC7A11 reciprocally regulated their expression via miR-1261 sponging by circ0097009.	Ferroptosis is involved in the progression of hepatocellular carcinoma through the circ0097009/miR-1261/SLC7A11 axis	2021	33987373
circSnx12	-	circRNA	-	mice	Heart Failure	Cardiac tissues	-	-	miR-224-5p	FTH1	circSnx12 Is Involved in Ferroptosis	we assessed the binding relationship between the ferroptosis-associated gene FTH1 and its target miR-224-5p. The results of luciferase reporter assay showed that miR-224-5p mimics could reduce the luciferase activity of FTH1 3'-UTR, but did not significantly affected that of FTH1 3'-UTR mutant. These findings imply that FTH1 is a direct target of miR-224-5p. Additionally, we demonstrated the regulatory relationship between miR-224-5p and circSnx12. 	circSnx12 Is Involved in Ferroptosis During Heart Failure by Targeting miR-224-5p	2021	33969020
circ_0007142	-	circRNA	cytoplasm	H.sapiens	Colorectal Cancer Cells	HCT116, SW620 and SW480	CCK-8 assay	-	miR-874-3p/GDPD5	-	Low circ_0007142 expression  accelerate of apoptosis	circ_0007142 was found as a miR-874-3p sponge and miR-874-3p inhibitor eliminated the regulation of si-circ_0007142 in CRC cells. MiR-874-3p targeted GDPD5 and upregulation of GDPD5 reversed the miR-874-3p-triggered tumour inhibition and ferroptosis promotion in CRC cells. Moreover, GDPD5 was regulated by the circ_0007142/miR-874-3p axis. Circ_0007142 also affected CRC tumorigenesis in vivo through the regulation of miR-874-3p and GDPD5.	Circ_0007142 downregulates miR-874-3p-mediated GDPD5 on colorectal cancer cells	2021	33797091
circRHOT1	-	circRNA	-	H.sapiens	Breast Cancer	MDA-MB-231 and T47D	MTT assays	-	miR-106a-5p/STAT3	STAT3	CircRHOT1 inhibits ferroptosis	the depletion of circRHOT1 enhanced the erastin-induced inhibition effect on cell growth of breast cancer cells. The circRHOT1 knockdown notably increased the levels of reactive oxygen species (ROS), iron, and Fe2+ in breast cancer cells. Mechanically, circRHOT1 was able to sponge microRNA-106a-5p (miR-106a-5p) and inhibited ferroptosis by down-regulating miR-106a-5p in breast cancer cells. Besides, miR-106a-5p induced ferroptosis by targeting signal transducer and activator of transcription 3 (STAT3) in the system. Moreover, the overexpression of STAT3 and miR-106a-5p inhibitor could reverse circRHOT1 knockdown-mediated breast cancer progression.	Circular RNA RHOT1 promotes progression and inhibits ferroptosis via mir-106a-5p/STAT3 axis in breast cancer	2021	33686957
circEPSTI1	-	circRNA	-	H.sapiens	Cervical Cancer	CaSki, HeLa, and HcerEpic	Liperfluo staining and confocal microscopy	-	miR-375/409-3P/515-5p-SLC7A11	GPX4	Silencing of circEPSTI1 induces ferroptosis	circEPSTI1 (hsa_circRNA_000479) was significantly upregulated in cervical cancer. We first discovered the impact of circRNA on cell ferroptosis in cervical cancer. Interestingly, circEPSTI1 attenuates the effect of ferritin which is mediated by SLC7A11 based on lipid peroxidation measurements and reduced glutathione and glutathione (GSH/GSSG) assay.	Circular RNA circEPSTI1 accelerates cervical cancer progression via miR-375/409-3P/515-5p-SLC7A11 axis	2021	33534779
circIL4R	-	circRNA	-	H.sapiens	Hepatocellular Carcinoma	THLE-2 and HuH-7	MTT assays	erastin	miR-541-3p/GPX4	ROS	CircIL4R knockdown impeded oncogenesis and expedited ferroptosis 	CircIL4R was abnormally overexpressed in HCC tissues and cells. CircIL4R knockdown impeded oncogenesis and expedited ferroptosis of HCC cells. CircIL4R could directly sponge microRNA-541-3p (miR-541-3p) and miR-541-3p inhibition mitigated the effects of circIL4R knockdown on HCC cells. CircIL4R acted as a miR-541-3p sponge to regulate its target glutathione peroxidase 4 (GPX4). GPX4 upregulation relieved the miR-541-3p-induced tumor inhibition and ferroptosis aggravation. CircIL4R played an oncogenic role in HCC via the miR-541-3p/GPX4 axis in vivo.	CircIL4R facilitates the tumorigenesis and inhibits ferroptosis in hepatocellular carcinoma by regulating the miR-541-3p/GPX4 axis	2020	32808701
cIARS	hsa_circ_0008367	circRNA	-	H.sapiens	Hepatocellular Carcinoma	HepG2, SMMC-7721, and Huh7	CCK-8 assay	SF or Erastin	ALKBH5	GSH	cIARS to be a positive regulator of ferroptosis	Prediction analysis and mechanistic identification revealed that cIARS physically interacted with RNA binding protein (RBP) ALKBH5, which was a negative regulator of autophagic flux in HCC. The dissociation of BCL-2/BECN1 complex, mediated by ALKBH5 silencing was effectively blocked by si-cIARS. Furthermore, the inhibition of ferroptotic events, autophagic flux and ferritinophagy resulted from si-cIARS, were significantly rescued by ALKBH5 downregulation.	Circular RNA cIARS regulates ferroptosis in HCC cells through interacting with RNA binding protein ALKBH5	2020	32802409
circABCB10	-	circRNA	-	H.sapiens	Rectal Cancer	SW837 and HR-8348 cell lines (up regulation)	CCK-8 assay, C11-BODIPY staining, flow cytometry, iron assay	Erastin	miR-326 / CCL5 (C-C motif chemokine ligand 5)	lipid ROS	circABCB10 deletion-induced cell ferroptosis and apoptosis	CircABCB10 performed carcinogenic functions to suppress ferroptosis and apoptosis in rectal cancer by regulating miR-326/CCL5 axis.	CircABCB10 silencing inhibits the cell ferroptosis and apoptosis by regulating the miR-326/CCL5 axis in rectal cancer	2020	32567935
circ-TTBK2	-	circRNA	-	H.sapiens	Glioma	LN229 and U251 cell lines (up regulation)	iron assay, lipid ROS assay, MTT assay	Erastin, Ferrostatin-1	miR-761 / ITGB8	lipid ROS	Circ-TTBK2 regulated cell proliferation, invasion and ferroptosis	Levels of circ-TTBK2 and ITGB8 were upregulated, whereas miR-761 level was low-expressed in glioma tissues and cells. CircTTBK2 was a sponge of miR-761 to modulate ITGB8. Additionally, circ-TTBK2 knockdown or miR-761 increase could retard cell proliferation, invasion, and promote ferroptosis in glioma cells. Interestingly, miR-761 inhibitor could abolish the repressive impact of circ-TTBK2 silencing on cell growth in vitro. Also, the influence of miR-761 mimic on cell phenotypes was regained after ITGB8 upregulation. Meanwhile, circ-TTBK2 deficiency caused the decrease of tumor growth.	Circ-TTBK2 regulated cell proliferation, invasion and ferroptosis via targeting ITGB8 by sponging miR-761 in glioma, providing a promising biomarker for the clinical therapy of human glioma.	2020	32196629
RP11-89	ENSG00000259439	lncRNA	-	H.sapiens	Bladder Cancer	5637 Cell and T24 Cell	CCK-8 assay, flow cytometry, Transwell assays, scratch tests and subcutaneous nude mouse models	-	TMEM161B-AS1-hsa-miR-27a-3p-FANCD2/CD44	iron export	positive	We demonstrated that RP11-89 is a novel tumorigenic regulator that inhibits ferroptosis via PROM2-activated iron export.	LncRNA RP11-89 facilitates tumorigenesis and ferroptosis resistance through PROM2-activated iron export by sponging miR-129-5p in bladder cancer	2021	34728613
TMEM161B-AS1	ENSG00000247828	lncRNA	-	H.sapiens	Glioma	U87 cells and U251 cells	qRT-PCR,Cell transfection,Dual luciferase reporter assay,Tumor xenograft assay,CCK-8 assay	-	TMEM161B-AS1-hsa-miR-27a-3p-FANCD2/CD44	lipid ROS	negative	Knockdown of TMEM161B-AS1 down-regulated the expression of FANCD2 and CD44 by sponging hsa-miR-27a-3p, inhibited the proliferation, migration, invasion and promoted apoptosis, ferroptosis of U87 cells and U251 cells. 	Over-expression of lncRNA TMEM161B-AS1 promotes the malignant biological behavior of glioma cells and the resistance to temozolomide via up-regulating the expression of multiple ferroptosis-related genes by sponging hsa-miR-27a-3p	2021	34689169
ZFAS1	ENSG00000177410	lncRNA	-	H.sapiens	Diabetic Cardiomyopathy	cardiomyocytes	Masson staining, immunohistochemical staining, Western blotting, monobromobimane staining, immunofluorescence staining and JC-1 staining	-	miR-150-5p/CCND2	GPX4	positive	Inhibition of ZFAS1 led to reduced collagen deposition, decreased cardiomyocyte apoptosis and ferroptosis, and attenuated DbCM progression. ZFAS1 sponges miR-150-5p to downregulate CCND2 expression.	Inhibition of the long non-coding RNA ZFAS1 attenuates ferroptosis by sponging miR-150-5p and activates CCND2 against diabetic cardiomyopathy	2021	34609043
Meg3	ENSMUSG00000021268	lncRNA	-	Rat	Diabetic Brain Ischemic Injury	microvascular endothelial cells	Cell transfection,RT-PCR,Iron concentration assay,lipid ROS assay,	-	p53/GPX4	GPX4	positive	Altogether, these data revealed that, by modulating GPX4 transcription and expression, the Meg3-p53 signaling pathway mediated the ferroptosis of RBMVECs upon injury induced by OGD combined with hyperglycemic reperfusion.	Long noncoding RNA Meg3 mediates ferroptosis induced by oxygen and glucose deprivation combined with hyperglycemia in rat brain microvascular endothelial cells, through modulating the p53/GPX4 axis	2021	34587716
PVT1	ENSG00000249859	lncRNA	cytoplasm	H.sapiens	Liver Cancer	HepG2 and Huh7	CCK-8 assay	ketamine, Erastin, or RSL3	miR-214-3p/GPX4	lipid ROS	Ferroptosis Induced by siPVT1	LncPVT1 directly interacted with miR-214-3p to impede its role as a sponge of GPX4. Depletion of lncPVT1 accelerated the ferroptosis of live cancer cells, whereas miR-214-3p inhibition and GPX4 overexpression reversed this effect. Ketamine-induced cell growth suppression and ferroptosis were also suppressed by miR-214-3p inhibition and GPX4 overexpression.	Ketamine Induces Ferroptosis of Liver Cancer Cells by Targeting lncRNA PVT1/miR-214-3p/GPX4	2021	34566408
H19	ENSG00000130600	lncRNA	cytoplasm	H.sapiens	Intracerebral Hemorrhage 	Brain microvascular endothelial cells	CCK-8 assay	erastin	miR-106b-5p	GSH	Knockdown of H19 promoted cell proliferation and suppressed BMVECs ferroptosis	Over-expression of H19 suppressed cell viability and promoted ferroptosis of BMVECs. miR-106b-5p is predicted to be a target of H19. The expression of miR-106b-5p was lower in oxygen and glucose deprivation hemin-treated (OGD/H-treated) cells. Over-expression of miR-106b-5p reversed the effects of H19 on cell viability and ferroptosis in BMVECs. Furthermore, acyl-CoA synthetase long-chain family member 4 (ACSL4) was verified to be a target gene of miR-106b-5p and was highly expressed in OGD/H-treated cells. Upregulation of ACSL4 inhibited the effects of miR-106b-5p and induced BMVEC dysfunction.	Long non-coding RNA H19 protects against intracerebral hemorrhage injuries via regulating microRNA-106b-5p/acyl-CoA synthetase long chain family member 4 axis	2021	34288826
OIP5-AS1	ENSG00000247556	lncRNA	-	H.sapiens	Prostate Cancer	PC3 and DU145 	MTT assay	Erastin and ferrostatin-1	miR-128-3p/SLC7A11	GSH	OIP5-AS1 promotes PCa progression and ferroptosis resistance	We found that lncRNA OIP5-AS1 expression was greatly elevated in PC3 and DU145 cells upon chronic Cd exposure. Dysregulation of OIP5-AS1 expression mediated cell growth and Cd-induced ferroptosis. Mechanistically, we demonstrated that OIP5-AS1 served as an endogenous sponge of miR-128-3p to regulate the expression of SLC7A11, a surrogate marker of ferroptosis. Moreover, miR-128-3p decreased cell viability by enhancing ferroptosis.	LncRNA OIP5-AS1 inhibits ferroptosis in prostate cancer with long-term cadmium exposure through miR-128-3p/SLC7A11 signaling	2021	34051661
HOTAIR	ENSG00000228630	lncRNA	cytoplasm	mice	Intracerebral Haemorrhage	HT22	MTT Assay	-	UPF1/ACSL4	ROS	HOTAIR overexpression reversed paeonol-induced inhibition of ferroptosis	Moreover, paeonol notably inhibited ferroptosis in hemin-treated neuronal cells via inhibition of ACSL4. Additionally, HOTAIR bound to UPF1, and UPF1 promoted the degradation of ACSL4 by binding to ACSL4. Furthermore, HOTAIR overexpression reversed paeonol-induced inhibition of ferroptosis by mediating the UPF1/ACSL4 axis. Paeonol inhibits the progression of ICH by mediating the HOTAIR/UPF1/ACSL4 axis.	Paeonol inhibits the progression of intracerebral haemorrhage by mediating the HOTAIR/UPF1/ACSL4 axis	2021	33906483
MEG8	ENSG00000225746	lncRNA	-	H.sapiens	Hemangioma	hemangioma endothelial cells	-	Ferrostatin-1	miR-497-5p/NOTCH2	GPX4	knockdown of MEG8 inhibited the proliferation and induced the ferroptosis	Knockdown of MEG8 increased the miR-497-5p expression and reduced the mRNA and protein levels of NOTCH2. Using a dual-luciferase assay, we confirmed the binding between MEG8 and miR-497-5p, and between the miR-497-5p and 3'UTR of NOTCH2. We further found that silencing MEG8 significantly decreased the expressions of SLC7A11 and GPX4 both in mRNA and protein level and had no effect on the level of AIFM2. Importantly, blocking miR-497-5p abrogated the effects of MEG8 loss on cell viability, MDA level and expression levels of NOTCH2, SLC7A11 and GPX4 in HemECs. Taken together, our results suggested that knockdown of long non-coding RNA MEG8 inhibited the proliferation and induced the ferroptosis of hemangioma endothelial cells by regulating miR-497-5p/NOTCH2 axis.	Silencing long non-coding RNA MEG8 inhibits the proliferation and induces the ferroptosis of hemangioma endothelial cells by regulating miR-497-5p/NOTCH2 axis	2021	33839417
NEAT1	ENSG00000245532	lncRNA	-	H.sapiens	Hbe And Nsclc	non-small-cell lung cancer	CCK8 assay	erastin	ACSL4	GPX4	NEAT1 regulates ferroptosis and ferroptosis sensitivity	Erastin-induced cell death was positively correlated with ACSL4 level. NEAT1 regulated levels of ACSL4 and proteins related to the ferroptosis and classical apoptosis pathways. Levels of ACSL4, SLC7A11, and GPX4 were decreased more by NEAT1 silencing plus erastin than by erastin alone.	Long non-coding RNA NEAT1 regulates ferroptosis sensitivity in non-small-cell lung cancer	2021	33730930
H19	ENSG00000130600	lncRNA	cytoplasm	H.sapiens	Spontaneous Abortio	placental villi tissues	-	Ferrostatin-1	Bcl-2 and GPX4	GPX4	H19 promoting apoptosis and ferroptosis	H19 expression was positively correlated with Bcl-2 and GPX4 expression and negatively linked with Bax levels. It was demonstrated that silencing H19 downregulated Bcl-2 and GPX4 expression and upregulated Bax expression at both the mRNA and protein levels in HTR-8/SVneo trophoblast cells. In conclusion, the present findings suggested that H19 has important roles in SA by promoting apoptosis and ferroptosis.	Long non-coding RNA H19 regulates Bcl-2, Bax and phospholipid hydroperoxide glutathione peroxidase expression in spontaneous abortion	2021	33273971
LINC00618	-	lncRNA	nucleus	H.sapiens	Leukemia	HL60 and K562	Iron Assay Kit	erastin	BAX	Lipid ROS	LINC00618 accelerates ferroptosis	LINC00618 promotes apoptosis by increasing the levels of BCL2-Associated X (BAX) and cleavage of caspase-3. LINC00618 also accelerates ferroptosis by increasing the levels of lipid reactive oxygen species (ROS) and iron, two surrogate markers of ferroptosis, and decreasing the expression of solute carrier family 7 member 11 (SLC7A11). Interestingly, VCR-induced ferroptosis and apoptosis are promoted by LINC00618, and LINC00618 accelerates ferroptosis in a manner dependent upon apoptosis. LINC00618 attenuates the expression of lymphoid-specific helicase (LSH), and LSH enhances the transcription of SLC7A11 after the recruitment to the promoter regions of SLC7A11, further inhibiting ferroptosis.	A Nuclear Long Non-Coding RNA LINC00618 Accelerates Ferroptosis in a Manner Dependent upon Apoptosis	2021	33002417
MT1DP	ENSG00000205361	lncRNA	-	H.sapiens	Non-Small Cell Lung Cancer	A549 and H1299	GSH assay kit	erastin	miR-365a-3p/NRF2	ROS	MT1DP attenuated expression of NRF2 and increased sensitivity of NRF2-overexpressed non-small cell lung cancer (NSCLC) cells to erastin-induced ferroptosis	In vivo analysis showed that E/M@FA-LPs had a favorable therapeutic effect on lung cancer xenografts. In short, our findings identify a novel strategy to elevate erastin-induced ferroptosis in NSCLCs acting through the MT1DP/miR-365a-3p/NRF2 axis.	MT1DP loaded by folate-modified liposomes sensitizes erastin-induced ferroptosis via regulating miR-365a-3p/NRF2 axis in non-small cell lung cancer cells	2020	32929075
PVT1	ENSG00000249859	lncRNA	cytoplasm	H.sapiens	Acute Ischemic Stroke	plasma	 GSH/GSSG	-	miR-214/p53	GPX4	PVT1 regulated ferroptosis	We found that the levels of PVT1 were upregulated and miR-214 levels were downregulated in plasma of AIS patients. NIHSS score was positively correlated with PVT1 levels but was negatively with miR-214 levels. PVT1 silencing or miR-214 overexpression significantly reduced infarct size and suppressed ferroptosis in vivo. miR-214 overexpression markedly decreased PVT1 levels. Specifically, miR-214 could bind to 3'untranslated region (3'UTR) of PVT1, TP53 or TFR1. PVT1 overexpression or miR-214 silencing markedly abolished the effects of Ferrostatin-1 on ferroptosis indicators except for TFR1 expression. Besides, miR-214 silencing counteracted the effects of PVT1 knockdown on the ferroptosis-related proteins.	LncRNA PVT1 regulates ferroptosis through miR-214-mediated TFR1 and p53	2020	32827544
ZFAS1	ENSG00000177410	lncRNA	cytoplasm	H.sapiens	Pulmonary Fibrosis	HFL1 cell line (up regulation)	lipid ROS assay, MDA assay, western blot	Ferrostatin-1	miR-150-5p / SLC38A1 (solute carrier family 38 member 1)	lipid ROS	silencing of lncRNA ZFAS1 attenuated ferroptosis	Silencing of lncRNA ZFAS1 attenuated ferroptosis and PF progression by lncRNA ZFAS1 acting as a competing endogenous RNA (ceRNA) and sponging miR-150-5p to downregulate SLC38A1 expression.	lncRNA ZFAS1 promotes lung fibroblast-to-myofibroblast transition and ferroptosis via functioning as a ceRNA through miR-150- 5p/SLC38A1 axis	2020	32453709
GABPB1-AS1	ENSG00000244879	lncRNA	cytoplasm	H.sapiens	Hepatocellular Carcinoma	HepG2, Huh7 and Hep3B cell lines (up regulation)	CCK-8 assay, lipid ROS assay, MDA assay	Erastin, Ferrostatin-1	GABPB1 (GA binding protein transcription factor subunit beta 1)	lipid ROS	Decreased GABPB1 expression levels during ferroptosis	GABPB1-AS1 was upregulated by erastin which inhibited the translation of GABPB1, leading to the inhibition of peroxidase gene expression and causing the accumulation of ROS and MDA and HepG2 cell death.	LncRNA GABPB1-AS1 and GABPB1 regulate oxidative stress during erastin-induced ferroptosis in HepG2 hepatocellular carcinoma cells	2019	31700067
RP11-274B21.9	-	lncRNA	-	H.sapiens	Lung Cancer	NCI-H1299 cell line (up regulation)	RNA-seq	-	SLC7A11	System Xc-	-	The lncRNA function analysis revealed that the ferroptosis pathway, which was associated with SLC7A11, was one of the significant pathways affected. The downregulation of SLC7A11 induced by XAV939 may suppress the development of NSCLC via the ferroptosis pathway.	RNA sequencing uncovers the key long non-coding RNAs and potential molecular mechanism contributing to XAV939-mediated inhibition of non-small cell lung cancer	2019	31186710
LINC00973	ENSG00000240476	lncRNA	-	H.sapiens	Lung Cancer	NCI-H1299 cell line (down regulation)	RNA-seq	-	SLC7A11	System Xc-	-	The lncRNA function analysis revealed that the ferroptosis pathway, which was associated with SLC7A11, was one of the significant pathways affected. The downregulation of SLC7A11 induced by XAV939 may suppress the development of NSCLC via the ferroptosis pathway.	RNA sequencing uncovers the key long non-coding RNAs and potential molecular mechanism contributing to XAV939-mediated inhibition of non-small cell lung cancer	2019	31186710
LINC00886	ENSG00000240875	lncRNA	-	H.sapiens	Lung Cancer	NCI-H1299 cell line (up regulation)	RNA-seq	-	SLC7A11	System Xc-	-	The lncRNA function analysis revealed that the ferroptosis pathway, which was associated with SLC7A11, was one of the significant pathways affected. The downregulation of SLC7A11 induced by XAV939 may suppress the development of NSCLC via the ferroptosis pathway.	RNA sequencing uncovers the key long non-coding RNAs and potential molecular mechanism contributing to XAV939-mediated inhibition of non-small cell lung cancer	2019	31186710
PCBP2-OT1	ENSG00000282977	lncRNA	-	H.sapiens	Lung Cancer	NCI-H1299 cell line (down regulation)	RNA-seq	-	SLC7A11	System Xc-	-	The lncRNA function analysis revealed that the ferroptosis pathway, which was associated with SLC7A11, was one of the significant pathways affected. The downregulation of SLC7A11 induced by XAV939 may suppress the development of NSCLC via the ferroptosis pathway.	RNA sequencing uncovers the key long non-coding RNAs and potential molecular mechanism contributing to XAV939-mediated inhibition of non-small cell lung cancer	2019	31186710
RP1-228H13.5	-	lncRNA	-	H.sapiens	Lung Cancer	NCI-H1299 cell line	RNA-seq	-	SLC7A11	System Xc-	-	The lncRNA function analysis revealed that the ferroptosis pathway, which was associated with SLC7A11, was one of the significant pathways affected. The downregulation of SLC7A11 induced by XAV939 may suppress the development of NSCLC via the ferroptosis pathway.	RNA sequencing uncovers the key long non-coding RNAs and potential molecular mechanism contributing to XAV939-mediated inhibition of non-small cell lung cancer	2019	31186710
LINC00336	ENSG00000197251	lncRNA	nucleus	H.sapiens	Lung Cancer	H358 and PC9 cell lines (up regulation)A549 and SPC-A-1 cell lines (down regulation)	MTT assay, iron assay, lipid ROS assay, MMP measurement, Mitosox Red staining, trypan blue staining	Erastin, RSL3, Ferrostatin-1	miR-6852 / CBS 	transsulfuration pathway	Overexpression of LINC00336 promotes cell growth, colony formation, tumor formation, and inhibits ferroptosis	LINC00336 functions as an oncogene to facilitate tumor cell proliferation, inhibit ferroptosis, and induce tumor formation in an ELAVL1-dependent manner.	Long noncoding RNA LINC00336 inhibits ferroptosis in lung cancer by functioning as a competing endogenous RNA	2019	30787392
P53RRA	ENSG00000233237	lncRNA	cytoplasm	H.sapiens	Lung Cancer	A549, SPCA1 and H522 cell lines (down regulation) HBE and H1299 cell lines (up regulation)	MTT assay, iron and ferrous iron assay, C11-BODIPY staining, flow cytometry	Erastin, Ferrostatin-1	G3BP1	lipid ROS	P53RRA promoted ferroptosis	LncRNAs can directly interact with the functional domain of signaling proteins in the cytoplasm, thus regulating p53 modulators to suppress cancer progression.	A G3BP1-interacting lncRNA promotes ferroptosis and apoptosis in cancer via nuclear sequestration of p53	2018	29588351
ASMTL-AS1	ENSG00000236017	lncRNA	nucleus and cytoplasm 	H.sapiens	Lung Adenocarcinoma	HLF-a, Calu-3, A549, NCI-H23 and SK-LU-1	CCK8 assay	-	SAT1	lipid ROS	ASMTL-AS1 positively regulated SAT1 to promote ferroptosis	mechanism assays were done to confirm the relationship among ASMTL-AS1, SAT1 and U2AF2. Results showed that ASMTL-AS1 was down-regulated in LUAD cells and ASMTL-AS1 up-regulation resulted in retarded LUAD cell and xenograft tumor growth along with stimulated ferroptosis. ASMTL-AS1 recruited U2AF2 to stabilize SAT1 mRNA. Furthermore, SAT1 exerted a cancer suppressor role in LUAD cells.	ASMTL-AS1 impedes the malignant progression of lung adenocarcinoma by regulating SAT1 to promote ferroptosis	2021	34658100
H19	ENSG00000130600	lncRNA	cytoplasm	H.sapiens	Breast Cancer	MCF7	CCK8 assay	erastin	-	glutathione assay kit	lncRNA-H19 can regulate both autophagy and ferroptosis	Autophagy inducers and H19 can reverse the production of lipid reactive oxygen species and the inhibition of autophagy induced by metformin. The present study suggests that metformin may induce ferroptosis by inhibiting autophagy via H19, and this discovery may facilitate the development of novel therapies for the treatment of breast cancer.	Metformin may induce ferroptosis by inhibiting autophagy via lncRNA H19 in breast cancer	2021	34644456
hsa-miR-15a-3p	MIMAT0004488	miRNA	-	H.sapiens	Colorectal Cancer	HCT-116, CaCo2, HT29, KM12 and NCM460	flow cytometer (Aceabio)	erastin	GPX4	GPX4	miR-15a-3p positively regulates ferroptosis	Here we identified miR-15a-3p positively regulates ferroptosis via directly targeting glutathione peroxidase glutathione peroxidase 4 (GPX4) in CRC. Overexpression of miR-15a-3p repressed GPX4 through binding to the 3'-untranslated region of GPX4, resulting in increased reactive oxygen species level, intracellular Fe2+ level, and malondialdehyde accumulation in vitro and in vivo. Correspondingly, suppression of miR-15a-3p reduced the sensitivity of CRC cells to erastin and GPX4. Taken together, these data demonstrate that miR-15a-3p regulates ferroptosis through targeting GPX4 in CRC cells, illustrating the novel role of microRNA in ferroptosis.	MiR-15a-3p regulates ferroptosis via targeting glutathione peroxidase GPX4 in colorectal cancer	2021	34727409
hsa-miR-539-5p	MIMAT0003163	miRNA	-	H.sapiens	Colorectal Cancer	HCT116 and SW480 and the 293T	CCK8 assay	-	TIPE	GPX4	miR-539 promotes ferroptosis by targeting TIPE	We aimed to investigate the functions and mechanisms of miR-539 in CRC proliferation. Functionally, miR-539 can bind to and regulate the expression of TIPE, and miR-539 activates SAPK/JNK to downregulate the expression of glutathione peroxidase 4 (GPX4) and promote ferroptosis. Our data reveal the novel role of miR-539 in regulating ferroptosis in CRC via activation of the SAPK/JNK axis, providing new insight into the mechanism of abnormal proliferation in CRC and a novel potential therapeutic target for advanced CRC.	miR-539 activates the SAPK/JNK signaling pathway to promote ferropotosis in colorectal cancer by directly targeting TIPE	2021	34601499
hsa-miR-7-5p	MIMAT0000252	miRNA	-	H.sapiens	Clinically Relevant Radioresistant	HeLa and SAS	MitoSOX<sup>TM</sup>	-	ALOX12	lipid ROS	miR-7-5p control radioresistance via ROS generation that leads to ferroptosis	Knockdown of miR-7-5p increased reactive oxygen species (ROS), mitochondrial membrane potential, and intracellular Fe2+ amount. Furthermore, miR-7-5p knockdown results in the down-regulation of the iron storage gene expression such as ferritin, up-regulation of the ferroptosis marker ALOX12 gene expression, and increases of Liperfluo amount. H2O2 treatment after ALOX12 overexpression led to the enhancement of intracellular H2O2 amount and lipid peroxidation. By contrast, miR-7-5p knockdown seemed not to be involved in COX-2 and glycolysis signaling but affected the morphology of CRR cells.	MiR-7-5p Is Involved in Ferroptosis Signaling and Radioresistance Thru the Generation of ROS in Radioresistant HeLa and SAS Cell Lines	2021	34361070
mmu-miR-15a	MIMAT0000526	miRNA	-	mice	Myocardial Infarctio	hearts	CCK8 assay	-	GPX4	GPX4	Over-expression of miR-15a-5p strengthened ferroptosis	Silencing transcription factor early growth response-1 (Egr-1) inhibited the level of miR-15a-5p, increased the protein expression of GPX4, accompanied by reduced ferroptosis and alleviated myocardial injury. In summary, these results provide a novel signaling pathway during the progression of acute myocardial infarction, namely Egr-1/miR-15a-5p/GPX4/ferroptosis.	The Egr-1/miR-15a-5p/GPX4 axis regulates ferroptosis in acute myocardial infarction	2021	34339707
hsa-miR-670-3p	MIMAT0026640	miRNA	-	H.sapiens	Glioblastoma	U87MG and A172, SVGp12 and HA1800	CCK8 assay	RSL3 or erastin	ACSL4	lipid ROS	microRNA-670-3p suppresses ferroptosis	miR-670-3p level was elevated in human glioblastoma, but decreased upon ferroptotic stimulation. miR-670-3p inhibitor suppressed, while miR-670-3p mimic promoted glioblastoma cell growth through modulating ferroptosis. Mechanistically, ACSL4 was required for the regulation on ferroptosis and growth of glioblastoma cells by miR-670-3p. Moreover, U87MG and A172 cells treated with miR-670-3p inhibitor showed an increased chemosensitivity to TMZ.	MicroRNA-670-3p suppresses ferroptosis of human glioblastoma cells through targeting ACSL4	2021	34323631
hsa-miR-302a-3p	MIMAT0000684	miRNA	-	H.sapiens	Non-Small Cell Lung Cancers		A549, H358, H1299 and H1650	Ferrostain-1/erastin/RSL3	FPN	lipid ROS	miR-302a-3p induce ferroptosis of NSCLCs	The miR-302a-3p mimic induced lipid peroxidation, iron overload and ferroptosis, thereby inhibiting cell growth and colony formation of NSCLCs cells. Conversely, the miR-302a-3p inhibitor block ederastin- or RSL3-related ferroptosis and tumor suppression. Additionally, we found that miR-302a-3p directly bound to the 3'-untranslational region of ferroportin to decrease its protein expression, and that ferroportin overexpression significantly prevented miR-302a-3p mimic-induced ferroptosis and tumor inhibition. Moreover, the miR-302a-3p mimic sensitized NSCLCs cells to cisplatin and paclitaxel chemotherapy.	MicroRNA-302a-3p induces ferroptosis of non-small cell lung cancer cells via targeting ferroportin	2021	34181495
hsa-miR-382-5p	MIMAT0000737	miRNA	-	H.sapiens	Ovarian And Breast Cancer	SKOV-3 and T47D	Apoptosis Assay Kit	lidocaine	SLC7A11	lipid ROS	inhibition of miR-382-5p blocked lidocaine-induced ferroptosis	MiR-382-5p/SLC7A11 axis was involved in lidocaine-mediated inhibition of ovarian and breast cancer cell proliferation in vitro. The miR-382-5p expression was down-regulated but SLC7A11 expression was up-regulated in clinical ovarian and breast cancer samples. Furthermore, the treatment of lidocaine repressed tumor growth of ovarian cancer cells in vivo, in which the miR-382-5p expression was increased while SLC7A11 expression was decreased. Consequently, we concluded that the lidocaine promoted ferroptosis by miR-382-5p/SLC7A11 axis in ovarian and breast cancer cells.	Lidocaine Promoted Ferroptosis by Targeting miR-382-5p /SLC7A11 Axis in Ovarian and Breast Cancer	2021	34122108
hsa-miR-130b-5p	MIMAT0004680	miRNA	-	H.sapiens		HTX1915, A375, G-361, HS1-CLS	CCK8 assay	erastin	DKK1	lipid ROS	miR-130b-3p to inhibit ferroptosis	The results indicated that miR-130b-3p exerted an inhibitory role in erastin or RSL3-induced ferroptosis, evidenced by reductions in lipid peroxidation and ferrous ion content. By suppressing the expression of target gene DKK1, miR-130b-3p activated the Nrf2/HO-1 pathway, whereby repressing ferroptosis. miR-130b-3p blocked the antitumor activity of erastin. Further, in vitro findings were reproduced in an in vivo murine model. Together, these data suggest the potential of miR-130b-3p to inhibit ferroptosis in melanoma cells and the mechanism was related to DKK1-mediated Nrf2/HO-1 pathway.	Suppressive role of microRNA-130b-3p in ferroptosis in melanoma cells correlates with DKK1 inhibition and Nrf2-HO-1 pathway activation	2021	34117611
hsa-miR-190a-5p	MIMAT0000458	miRNA	-	H.sapiens	Myocardial Infarction	H9c2 cells and HEK-293	Lipid Peroxidation (MDA) Assay Kit	erastin and RSL3	GLS2	lipid ROS	miR-190a-5p negatively regulate ferroptosis 	We found that miR-190a-5p negatively regulate ferroptosis via directly targeting GLS2 in rat cardiomyocyte H9c2 cells. Forced expression of miR-190a-5p inhibited GLS2, resulting in downregulation of ROS, MDA and Fe 2+ accumulation. Meanwhile, inhibition of miR-190a-5p caused upregulation of GLS2, resulting in opposite effects which could be blocked by GLS2 inhibitor compound 968.	miR-190a-5p regulates cardiomyocytes response to ferroptosis via directly targeting GLS2	2021	34111670
hsa-miR-375-3p	MIMAT0000728	miRNA	-	H.sapiens	Gastric Cancer	SGC-7901 and BGC-823	CCK8 assay	erastin, sorafenib, sulfasalazine	SLC7A11	lipid ROS	MiR-375 can trigger the ferroptosis	microarray and bioinformatics analysis were performed to search the potential targets of miR-375 in GC cells. Luciferase reporter, RNA immunoprecipitation, and RNA-FISH assays were carried out to verify the targeting of miR-375. Subsequently, combined with tissue microarray analysis, erastin-resistant GC cells, transmission electron microscopy, a series of agonists and oxidative stress markers, the underlying mechanisms contributing to miR-375-mediated effects were explored.	MiR-375 reduces the stemness of gastric cancer cells through triggering ferroptosis	2021	34090492
mmu-miR-122-5p	MIMAT0000246	miRNA	-	Mouse	Intracerebral Hemorrhage	HT-22 cell	CCK8 assay	erastin	TP53/SLC7A11	Lipid ROS	IRN could alleviate ferroptosis-induced neurological damage after ICH through upregulating miR-122-5p	Cells were treated with IRN following treatment with FAC after transfection with miR-122-5p inhibitor, and the results showed IRN reduced the FAC-induced decrease of miR-122-5p levels and relieved the ferroptosis by detecting ferroptotic marker proteins, iron ion concentration and oxidative stress level; after transfection with miR-122-5p inhibitor, the protective effects of IRN against FAC-induced ferroptosis in these cells were weakened. TP53 (also known as p53) was verified as a target of miR-122-5p by using dual luciferase reporter assay, and restoration of TP53 attenuated the effects of miR-122-5p on ferroptotic marker proteins expression, iron ion concentration and lipid ROS levels, as well as solute carrier family seven member 11 (SLC7A11) mRNA expression.	Isorhynchophylline Relieves Ferroptosis-Induced Nerve Damage after Intracerebral Hemorrhage Via miR-122-5p/TP53/SLC7A11 Pathway	2021	33942214
hsa-miR-4443	MIMAT0018961	miRNA	-	H.sapiens	Non-Small Cell Lung Carcinoma	Exosomes	CCK8 assay	erastin	METTL3	Lipid ROS	miR-4443 inhibited FSP1-mediated ferroptosis	Through bioinformatics analysis and luciferase assays, METTL3 was confirmed as a direct target gene of miR-4443. Further mechanistic analysis showed that miR-4443 regulated the expression of FSP1 in an m6A manner via METLL3.	Exosomal miR-4443 promotes cisplatin resistance in non-small cell lung carcinoma by regulating FSP1 m6A modification-mediated ferroptosis	2021	33781830
circKDM4C	-	circRNA	-	H.sapiens	Acute Myeloid Leukemia	K-562 and HL-60	CCK8 assay	erastin	hsa-let-7b-5p/p53	Lipid ROS	circKDM4C induces ferroptosis by sponging hsa-let-7b-5p	We found that circKDM4C acts as a sponge of hsa-let-7b-5p and thereby regulates p53 which is a target gene of hsa-let-7b-5p. Also, the expression of circKDM4C and hsa-let-7b-5p are negatively correlated, while circKDM4C and p53 are positively correlated to AML patients. Moreover, we found that circKDM4C induces ferroptosis by sponging hsa-let-7b-5p which upregulates the expression of P53. 	CircKDM4C upregulates P53 by sponging hsa-let-7b-5p to induce ferroptosis in acute myeloid leukemia	2021	33733556
hsa-miR-101-3p	MIMAT0000099	miRNA	-	H.sapiens	Pulmonary Cancer	A549, L78, NCI-H460, GLC-82, SPC-A1, and PC9	CCK8 assay	-	TBLR1	ROS	miR-101-3p restores ferroptosis	The expression levels of miR-101-3p and its target protein TBLR1 in tumour tissues and cells were detected, and their relationship with ferroptosis was clarified. Furthermore, the efficacy of nanocarriers in achieving in vivo therapeutic gene delivery was evaluated. Nanomedicine was further developed, with the anti-proliferative in vivo therapeutic effect validated using a subcutaneous xenograft cancer model. The expression level of miR-101-3p negatively correlated with clinical tumour size and TNM stage. miR-101-3p restores ferroptosis in tumour cells by directly targeting TBLR1, which in turn promotes apoptosis and inhibits proliferation.	Nanomedicine promotes ferroptosis to inhibit tumour proliferation in vivo	2021	33674250
hsa-miR-324-3p	MIMAT0000762	miRNA	-	H.sapiens	Non Small Cell Lung Cancer	A549/DDP	CCK8 assay	-	GPX4	ROS	miR-324-3p enhanced cisplatin-induced ferroptosis in the A549/DDP cells	We identified the glutathione peroxidase 4 (GPX4) gene as the direct target of miR-324-3p, where overexpression of the gene reversed the miR-324-3p effect of sensitizing the A549/DDP cells to cisplatin. Furthermore, the GPX4 inhibitor RSL3 could mimic the effect of miR-324-3p upregulation in increasing the sensitivity of the cisplatin-resistant cells to the drug. Significantly, miR-324-3p enhanced cisplatin-induced ferroptosis in the A549/DDP cells.	miR-324-3p reverses cisplatin resistance by inducing GPX4-mediated ferroptosis in lung adenocarcinoma cell line A549	2021	33662669
rno-miR-335	MIMAT0000575	miRNA	-	rats	Parkinson'S Disease	PC12 cells	MMP assay	-	FTH1	ROS	miR-335 enhanced ferroptosis	The luciferase 3'-untranslated region reporter results identified FTH1 as the direct target of miR-335. The silencing of FTH1 in 6-OHDA-stimulated cells enhanced the effects of miR-335 on ferroptosis and promoted PD pathology. Mechanistically, miR-335 enhanced ferroptosis through the degradation of FTH1 to increase iron release, lipid peroxidation and reactive oxygen species (ROS) accumulation, and to decrease mitochondrial membrane potential (MMP). 	miR‑335 promotes ferroptosis by targeting ferritin heavy chain 1 in in vivo and in vitro models of Parkinson's disease	2021	33649797
hsa-miR-324-3p	MIMAT0000762	miRNA	-	H.sapiens	Breast Cancer	MDA-MB-231 and MCF-7	BX53M fluorescence microscope	erastin	GPX4	ROS	metformin induced ferroptosis by upregulating miR-324-3p	Overexpression of miR-324-3p inhibited cancer cell viability. miR-324-3p inhibitor promoted cell viability. Further studies showed that the effect of miR-324-3p was mediated by directly targeting glutathione peroxidase 4 (GPX4). miR-324-3p bound to the 3ʹ-UTR of GPX4 and led to the downregulation of GPX4. In vivo studies showed that metformin induced ferroptosis by upregulating miR-324-3p in the xenograft model of breast cancer in mice.	Metformin induces ferroptosis by targeting miR-324-3p/GPX4 axis in breast cancer	2021	33522578
rno-miR-23a-3p	MIMAT0000792	miRNA	-	rats	Intracerebral Hemorrhage	Brain	-	-	NFE2L2	ROS	miR-23a-3p Inhibition Attenuates the Ferroptosis	Acupuncture also alleviated ferroptosis and decreased miR-23a-3p expression, as evidenced by the increased NFE2L2 nuclear translocation and expressions of heme oxygenase-1 and glutathione peroxidase 4 and the decreased iron and malondialdehyde contents and reactive oxygen species accumulation. Additionally, antagomiR-23a-3p inhibited the ICH-induced increases in FJB-positive cells, release of proinflammatory cytokines, ferroptosis, and promoted NFE2L2 activation. Notably, the binding site of miR-23a-3p existed in NFE2L2. Taken together, acupuncture may alleviate the neuronal cell death, inflammation, and ferroptosis after ICH by down-regulating miR-23a-3p.	Acupuncture Ameliorates Neuronal Cell Death, Inflammation, and Ferroptosis and Downregulated miR-23a-3p After Intracerebral Hemorrhage in Rats	2021	33403590
hsa-miR-10a-5p	MIMAT0000253	miRNA	-	H.sapiens	Intervertebral Disc Degeneration	chondrocytes	DCFH-DA	-	IL-6R	ROS	Overexpressing miR-10a-5p suppressed IL-6R expression, and partially abolished IL-6-induced ferroptosis	Results from current study suggests that inflammatory cytokine IL-6 appeared in IVD aggravates its degeneration by inducing cartilage cell ferroptosis. This is caused partially by inhibiting miR-10a-5p and subsequently derepressing IL-6R signaling pathway. Our study provides a novel mechanism explaining inflammatory cytokine-caused cartilage cell death in degenerative IVD, and makes IL-6/miR-10a-5p/IL-6R axis a potential therapeutic target for intervention of IDD.	Targeting miR-10a-5p/IL-6R axis for reducing IL-6-induced cartilage cell ferroptosis	2020	33166496
mmu-miR-182-5p	MIMAT0000211	miRNA	-	mouse	Ischemia/Reperfusion (I/R) Kidney Injury	TCMK-1 	Iron Assay Kit (Abcam)	erastin/ferrostatin-1	GPX4	ROS	miR-182-5p and miR-378a-3p induced ferroptosis	We identified that miR-182-5p and miR-378a-3p were upregulated in the ferroptosis and H/R-induced injury, and correlates reversely with glutathione peroxidases 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) expression in renal I/R injury tissues, respectively. In vitro studies showed that miR-182-5p and miR-378a-3p induced ferroptosis in cells. We further found that miR-182-5p and miR-378a-3p regulated the expression of GPX4 and SLC7A11 negatively by directly binding to the 3'UTR of GPX4 and SLC7A11 mRNA. In vivo study showed that silencing miR-182-5p and miR-378a-3p alleviated the I/R-induced renal injury in rats.	miR-182-5p and miR-378a-3p regulate ferroptosis in I/R-induced renal injury	2020	33116120
mmu-miR-378a-3p	MIMAT0003151	miRNA	-	mouse	Ischemia/Reperfusion (I/R) Kidney Injury	TCMK-1 	Iron Assay Kit (Abcam)	erastin/ferrostatin-1	SLC7A11	ROS	miR-182-5p and miR-378a-3p induced ferroptosis	We identified that miR-182-5p and miR-378a-3p were upregulated in the ferroptosis and H/R-induced injury, and correlates reversely with glutathione peroxidases 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) expression in renal I/R injury tissues, respectively. In vitro studies showed that miR-182-5p and miR-378a-3p induced ferroptosis in cells. We further found that miR-182-5p and miR-378a-3p regulated the expression of GPX4 and SLC7A11 negatively by directly binding to the 3'UTR of GPX4 and SLC7A11 mRNA. In vivo study showed that silencing miR-182-5p and miR-378a-3p alleviated the I/R-induced renal injury in rats.	miR-182-5p and miR-378a-3p regulate ferroptosis in I/R-induced renal injury	2020	33116120
hsa-miR-137-3p	MIMAT0000429	miRNA	-	H.sapiens	Neuroblastoma	SH-SY5Y cells 	MTT assay	oxyHb	COX2/PGE2	ROS	decrease in miR-137 levels and inhibit ferroptosis	miR-137 overexpression boosts the neuroprotective effects of EPC-EXs against apoptosis and mitochondrial dysfunction in oxyHb-treated SH-SY5Y cells. Furthermore, EXsmiR-137 rather than EXs can restore the decrease in miR-137 levels and inhibit ferroptosis, and the protection mechanism might involve the miR-137-COX2/PGE2 signaling pathway.	miR-137 boosts the neuroprotective effect of endothelial progenitor cell-derived exosomes in oxyhemoglobin-treated SH-SY5Y cells partially via COX2/PGE2 pathway	2020	33100224
hsa-miR-424-5p	MIMAT0001341	miRNA	-	H.sapiens	Ovarian Cancer	ovarian	iron assay kit	erastin	ACSL4	ACSL4	miR-424-5p regulates ferroptosis by targeting ACSL4 in ovarian cancer cells	We show that miR-424-5p negatively regulates ferroptosis by directly targeting ACSL4 in ovarian cancer cells. Upregulation of miR-424-5p suppressed ACSL4 by directly binding to its 3'-UTR, which subsequently reduced erastin- and RSL3-induced ferroptosis. Meanwhile, knockdown of miR-424-5p increased the sensitivity of ovarian cancer cells to erastin and RSL3. Furthermore, ACSL4 was upregulated in ovarian cancer tissues, and high ACSL4 expression predicted worse prognosis and sensitized ovarian cancer cells to erastin- and RSL3-induced ferroptosis. Importantly, decreases in lipid peroxides and ferroptotic cell death mediated by miR-424-5p could be abrogated by ACSL4 overexpression.	Tumor suppressor miR-424-5p abrogates ferroptosis in ovarian cancer through targeting ACSL4	2020	33038905
hsa-miR-522	MI0003177	miRNA	exosomes	H.sapiens	Gastric Cancer	cancer-associated fibroblast (CAF) cell lines (up regulation)	mass spectrum, RT-qPCR, lipid ROS assay, MMP measurement	Erastin	ALOX15 (arachidonate lipoxygenase 15)	lipid ROS	miR-522 suppresses ferroptosis	CAFs secrete exosomal miR-522 to inhibit ferroptosis in cancer cells by targeting ALOX15 and blocking lipid-ROS accumulation. Importantly, cisplatin and paclitaxel promote miR-522 secretion from CAFs by activating USP7/hnRNPA1 axis and ultimately result in decreased chemo-sensitivity.	CAF secreted miR-522 suppresses ferroptosis and promotes acquired chemo-resistance in gastric cancer	2020	32106859
hsa-miR-214	MI0000290	miRNA	-	H.sapiens	Hepatoma	HepG2 and Hep3B cell lines (down regulation)	CCK-8 assay, colony formation assay, iron assay, MDA assay, DCFH-DA  staining, flow cytometry	Erastin, Ferrostatin-1	ATF4 (transcription factor 4)	lipid ROS	microRNA-214-3p enhances erastin-induced ferroptosis	The ferroptosis-promoting effects of miR-214 in hepatoma cells are attributed at least to its inhibitory effects on ATF4, which may provide a new target for therapy of hepatoma regarding ferroptosis.	MicroRNA-214-3p enhances erastin-induced ferroptosis by targeting ATF4 in hepatoma cells	2020	31960438
hsa-miR-30b-5p	MIMAT0000420	miRNA	-	H.sapiens	Preeclampsia	HTR-8/SVneo and TEV-1	H2DCFDA	-	Pax3/SLC7A11	GPX4	upregulation of miR-30b-5p in PE models plays a pivotal role in ferroptosis	Microarrays, bioinformatic analysis, and luciferase reporter assay revealed that upregulation of miR-30b-5p in PE models plays a pivotal role in ferroptosis, by downregulating Cys2/glutamate antiporter and PAX3 and decreasing ferroportin 1 (an iron exporter) expression, resulting in decreased GSH and increased labile Fe2+. Inhibition of miR-30b-5p expression and supplementation with ferroptosis inhibitors attenuated the PE symptoms in rat models, making miR-30b-5p a potential therapeutic target for PE.	miR-30-5p-mediated ferroptosis of trophoblasts is implicated in the pathogenesis of preeclampsia	2020	31926626
hsa-miR-4715-3p	MIMAT0019825	miRNA	-	H.sapiens	Gastric Cancer, Esophagus Cancer	OE33, MKN45 and STKM2 cell lines (down regulation)	western blot, qRT-PCR, luciferase reporter assay, flow cytometry	-	AURKA (Aurora kinase A)	GPX4	miR-4715-3p inhibited GPX4 and induced cell death, suggesting a link between AURKA and ferroptosis	Inhibition of AURKA or reconstitution of miR-4715-3p induced cell death and inhibited GPX4. miR-4715-3p reconstitution enhanced cisplatin sensitivity.	Epigenetic regulation of AURKA by miR-4715-3p in upper gastrointestinal cancers	2019	31740746
hsa-miR-103a-3p	MIMAT0000101	miRNA	-	H.sapiens	Gastric Cancer	MGC-803 and MKN-45 cell lines (up regulation)	CCK-8 assay, lipid ROS assay, MDA assay, iron assay	Erastin, Ferrostatin-1	GLS2 (glutaminase 2)	glutamine metabolism	PG exerts pro-ferroptosis and anti-tumor effects in vitro and in vivo through regulating miR-103a-3p/GLS2 axis	PG treatment significantly promoted ferroptosis and anti-tumorigenesis by down-regulating inhibitory effect of miR-103a-3p on GLS2 expression.	Physcion 8-O-β-glucopyranoside induced ferroptosis via regulating miR-103a-3p/GLS2 axis in gastric cancer	2019	31606381
hsa-miR-212-5p	MIMAT0022695	miRNA	extracellular vesicle	mice	Tbi (Traumatic Brain Injury)	HT-22 and Neuro-2a cell lines (down regulation)	qRT-PCR, western blot, iron assay, MDA assay	RSL3, Ferrostatin-1	Ptgs2 (prostaglandin-endoperoxide synthase-2)	lipid ROS	overexpression of miR-212-5p attenuated ferroptosis	miR-212-5p was significantly downregulated after TBI and functionally suppressed ferroptosis by directly targeting Ptgs2. Administration of miR-212-5p in CCI mice significantly improved learning and spatial memory.	miR-212-5p attenuates ferroptotic neuronal death after traumatic brain injury by targeting Ptgs2	2019	31533781
hsa-miR-7-5p	MIMAT0000252	miRNA	-	H.sapiens	Cervical Cancer, Tongue Squamous Carcinoma, Hepatoma	CRR (clinically relevant radioresistant) cells in HeLa, SAS and HepG2 cell lines (up regulation)	FerroOrange	-	-	iron metabolism	miR-7-5p downregulates mitoferrin and reduces Fe2+, which influences ferroptosis	MiR-7-5p may control radioresistance in various cancer cells at the clinically relevant dose of irradiation. MiR-7-5p downregulates mitoferrin and reduces Fe2+, which influences ferroptosis. 	MiR-7-5p is a key factor that controls radioresistance via intracellular Fe2+ content in clinically relevant radioresistant cells	2019	31472959
hsa-miR-17	MI0000071	miRNA	endothelial cell	H.sapiens	-	HUVEC cell line (up regulation)	CCK-8 assay, C11-BODIPY staining, flow cytometry	Erastin, Ferrostatin-1	A20 (known as TNFAIP3) / ACSL4	lipid ROS	miR-17-92 protects endothelial cells from erastin-induced ferroptosis by targeting the A20-ACSL4 axis	This study revealed a novel mechanism through which miR-17-92 protects endothelial cells from erastin-induced ferroptosis by targeting the A20-ACSL4 axis.	miRNA-17-92 protects endothelial cells from erastin-induced ferroptosis through targeting the A20-ACSL4 axis	2019	31160087
hsa-miR-18a	MI0000072	miRNA	endothelial cell	H.sapiens	-	HUVEC cell line (up regulation)	CCK-8 assay, C11-BODIPY staining, flow cytometry	Erastin, Ferrostatin-1	A20 (known as TNFAIP3) / ACSL4	lipid ROS	miR-17-92 protects endothelial cells from erastin-induced ferroptosis by targeting the A20-ACSL4 axis	This study revealed a novel mechanism through which miR-17-92 protects endothelial cells from erastin-induced ferroptosis by targeting the A20-ACSL4 axis.	miRNA-17-92 protects endothelial cells from erastin-induced ferroptosis through targeting the A20-ACSL4 axis	2019	31160087
hsa-miR-19a	MI0000073	miRNA	endothelial cell	H.sapiens	-	HUVEC cell line (up regulation)	CCK-8 assay, C11-BODIPY staining, flow cytometry	Erastin, Ferrostatin-1	A20 (known as TNFAIP3) / ACSL4	lipid ROS	miR-17-92 protects endothelial cells from erastin-induced ferroptosis by targeting the A20-ACSL4 axis	This study revealed a novel mechanism through which miR-17-92 protects endothelial cells from erastin-induced ferroptosis by targeting the A20-ACSL4 axis.	miRNA-17-92 protects endothelial cells from erastin-induced ferroptosis through targeting the A20-ACSL4 axis	2019	31160087
hsa-miR-20a	MI0000076	miRNA	endothelial cell	H.sapiens	-	HUVEC cell line (up regulation)	CCK-8 assay, C11-BODIPY staining, flow cytometry	Erastin, Ferrostatin-1	A20 (known as TNFAIP3) / ACSL4	lipid ROS	miR-17-92 protects endothelial cells from erastin-induced ferroptosis by targeting the A20-ACSL4 axis	This study revealed a novel mechanism through which miR-17-92 protects endothelial cells from erastin-induced ferroptosis by targeting the A20-ACSL4 axis.	miRNA-17-92 protects endothelial cells from erastin-induced ferroptosis through targeting the A20-ACSL4 axis	2019	31160087
hsa-miR-19b	MI0000074	miRNA	endothelial cell	H.sapiens	-	HUVEC cell line (up regulation)	CCK-8 assay, C11-BODIPY staining, flow cytometry	Erastin, Ferrostatin-1	A20 (known as TNFAIP3) / ACSL4	lipid ROS	miR-17-92 protects endothelial cells from erastin-induced ferroptosis by targeting the A20-ACSL4 axis	This study revealed a novel mechanism through which miR-17-92 protects endothelial cells from erastin-induced ferroptosis by targeting the A20-ACSL4 axis.	miRNA-17-92 protects endothelial cells from erastin-induced ferroptosis through targeting the A20-ACSL4 axis	2019	31160087
hsa-miR-92	-	miRNA	endothelial cell	H.sapiens	-	HUVEC cell line (up regulation)	CCK-8 assay, C11-BODIPY staining, flow cytometry	Erastin, Ferrostatin-1	A20 (known as TNFAIP3) / ACSL4	lipid ROS	miR-17-92 protects endothelial cells from erastin-induced ferroptosis by targeting the A20-ACSL4 axis	This study revealed a novel mechanism through which miR-17-92 protects endothelial cells from erastin-induced ferroptosis by targeting the A20-ACSL4 axis.	miRNA-17-92 protects endothelial cells from erastin-induced ferroptosis through targeting the A20-ACSL4 axis	2019	31160087
hsa-miR-9	-	miRNA	-	H.sapiens	Melanoma	A375 and G-361 cell lines (up regulation)	CCK-8 assay, MDA assay, iron assay, glutamate assay, glutamine assay, a-KG assay	Erastin, RSL3, Ferrostatin-1	GOT1	glutaminolysis	miR-9 regulates ferroptosis by targeting GOT1	Overexpression of miR-9 suppressed GOT1 by directly binding to its 3'-UTR, which subsequently reduced erastin- and RSL3-induced ferroptosis.	miR-9 regulates ferroptosis by targeting glutamic-oxaloacetic transaminase GOT1 in melanoma	2018	30035324
hsa-miR-137	MI0000454	miRNA	-	H.sapiens	Melanoma	A375 and G-361 cell lines (up regulation)	CCK-8 assay, MDA assay, C11-BODIPY staining, flow cytometry, iron assay, glutamine uptake assay	Erastin, RSL3, Ferrostatin-1	SLC1A5	glutaminolysis	knockdown of miR-137 increased the antitumor activity of erastin by enhancing ferroptosis	MiR-137 negatively regulates ferroptosis by directly targeting glutamine transporter SLC1A5 in melanoma cells.	miR-137 regulates ferroptosis by targeting glutamine transporter SLC1A5 in melanoma	2018	29348676
hsa-miR-27a-3p	MIMAT0000084	miRNA	-	H.sapiens	Non-Small Cell Lung Cancer	Beas-2B	CCK-8 assay	erastin	SLC7A11	ROS	miR-27a-3p modulated ferroptosis by targeting SLC7A11 in NSCLC cells	miR-27a-3p, was an essential modulator of ferroptosis via directly targeting SLC7A11 in NSCLC cells. Overexpressing miR-27a-3p led to SLC7A11 suppression via directly binding to its 3'-UTR, followed by the reduction of erastin-caused ferroptosis. In contrast, inhibited miR-27a-3p resulted in an increase in NSCLC cells' sensitivity to erastin. Of importance, the accumulated lipid ROS and cell death of iron peptide mediated by anti-miR-27a-3p can be eliminated by impeding the glutamylation process.	MiR-27a-3p Promotes Non-Small Cell Lung Cancer Through SLC7A11-Mediated-Ferroptosis	2021	34722314
hsa-miR-5096	MIMAT0020603	miRNA	-	H.sapiens	Breast Cancer	MDA-MB-468, MDA-MB-453, BT-549, MDAMB-231, SKBR-3, T-47D, MCF-7, and ZR-75 and a normal epithelial breast cell line, MCF-10A	ferene assay	erastin	SLC7A11/ xCT	SLC7A11	miR-5096-induced ferroptotic cell death	We demonstrated SLC7A11 as a target of miR-5096 by 3'UTR luciferase assay and further validated it by identifying reduced mRNA and protein levels of SLC7A11 upon miR-5096 overexpression. miR-5096-induced ferroptotic cell death in human breast cancer cells was confirmed by concurrently increased ROS, OH-, lipid ROS, and iron accumulation levels and decreased GSH and mitochondrial membrane potential with mitochondrial shrinkage and partial cristae loss.	SLC7A11/ xCT is a target of miR-5096 and its restoration partially rescues miR-5096-mediated ferroptosis and anti-tumor effects in human breast cancer cells	2021	34571083
hsa-miR-34a-5p	MIMAT0000255	miRNA	-	H.sapiens		PC12	MTT assay/DCFH-DA		Sirt1	lipid ROS	Knock-down of miR-34a-5p mitigates CdCl2-induced ferroptosis	The molecular mechanisms leading to apoptosis and ferroptosis at least included the participation of the miR-34a-5p/Sirt1 axis, in which miR-34a-5p promoted CdCl2 -induced neurotoxicity through targeting Sirt1. Knocking out miR-34a-5p attenuated CdCl2 -induced damage of PC12 cells, cytotoxicity and neurotoxicity.	Cadmium induces ferroptosis and apoptosis by modulating miR-34a-5p/Sirt1axis in PC12 cells	2021	34558789
mmu-miR-124-3p	MIMAT0000134	miRNA	-	Mouse	Aged Intracerebral Hemorrhage	Serum	-	-	Fpn	-	miR124/Fpn signaling may mediate the outcome of ICH through apoptosis and ferroptosis	Based on prediction of website tools, expression level of potential miRNAs in ICH tissues and results of luciferase reporter assays, miR-124 was identified to regulate Fpn expression post-ICH. Higher serum miR-124 levels were correlated with poor neurologic scores of aged ICH patients. Administration of miR-124 antagomir enhanced Fpn expression and attenuated iron accumulation in aged mice model. Both apoptosis and ferroptosis, but not necroptosis, were regulated by miR-124/Fpn signaling manipulation.	Targeting miR-124/Ferroportin signaling ameliorated neuronal cell death through inhibiting apoptosis and ferroptosis in aged intracerebral hemorrhage murine model	2020	33068460
hsa-miR-19b-3p	MIMAT0000074	miRNA	-	H.sapiens	Colorectal Cancer	CaCO2 cell line (up regulation)	miScript System (miRNA PCR Array miFinder)	Erastin	ACSL4	lipid ROS	elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2 cells compared to in DLD-1 cells potentially targeted ACSL-4 	Interactome analysis between these down-regulated gene and up-regulated miRNAs altered by bromelain in CaCO2 cells compared to in DLD-1 cells indicated that ACSL-4 is a key regulatory molecule.	Bromelain effectively suppresses Kras-mutant colorectal cancer by stimulating ferroptosis	2018	30460115
hsa-miR-130a-3p	MIMAT0000425	miRNA	-	H.sapiens	Colorectal Cancer	CaCO2 cell line (up regulation)	miScript System (miRNA PCR Array miFinder)	Erastin	ACSL4	lipid ROS	elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2 cells compared to in DLD-1 cells potentially targeted ACSL-4 	Interactome analysis between these down-regulated gene and up-regulated miRNAs altered by bromelain in CaCO2 cells compared to in DLD-1 cells indicated that ACSL-4 is a key regulatory molecule.	Bromelain effectively suppresses Kras-mutant colorectal cancer by stimulating ferroptosis	2018	30460115
hsa-miR-150-5p	MIMAT0000451	miRNA	-	H.sapiens	Colorectal Cancer	CaCO2 cell line (up regulation)	miScript System (miRNA PCR Array miFinder)	Erastin	ACSL4	lipid ROS	elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2 cells compared to in DLD-1 cells potentially targeted ACSL-4 	Interactome analysis between these down-regulated gene and up-regulated miRNAs altered by bromelain in CaCO2 cells compared to in DLD-1 cells indicated that ACSL-4 is a key regulatory molecule.	Bromelain effectively suppresses Kras-mutant colorectal cancer by stimulating ferroptosis	2018	30460115
hsa-miR-144-3p	MIMAT0000436	miRNA	-	H.sapiens	Colorectal Cancer	CaCO2 cell line (up regulation)	miScript System (miRNA PCR Array miFinder)	Erastin	ACSL4	lipid ROS	elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2 cells compared to in DLD-1 cells potentially targeted ACSL-4 	Interactome analysis between these down-regulated gene and up-regulated miRNAs altered by bromelain in CaCO2 cells compared to in DLD-1 cells indicated that ACSL-4 is a key regulatory molecule.	Bromelain effectively suppresses Kras-mutant colorectal cancer by stimulating ferroptosis	2018	30460115
hsa-miR-16-5p	MIMAT0000069	miRNA	-	H.sapiens	Colorectal Cancer	CaCO2 cell line (up regulation)	miScript System (miRNA PCR Array miFinder)	Erastin	ACSL4	lipid ROS	elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2 cells compared to in DLD-1 cells potentially targeted ACSL-4 	Interactome analysis between these down-regulated gene and up-regulated miRNAs altered by bromelain in CaCO2 cells compared to in DLD-1 cells indicated that ACSL-4 is a key regulatory molecule.	Bromelain effectively suppresses Kras-mutant colorectal cancer by stimulating ferroptosis	2018	30460115
hsa-miR-7a-5p	-	miRNA	-	H.sapiens	Colorectal Cancer	CaCO2 cell line (up regulation)	miScript System (miRNA PCR Array miFinder)	Erastin	ACSL4	lipid ROS	elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2 cells compared to in DLD-1 cells potentially targeted ACSL-4 	Interactome analysis between these down-regulated gene and up-regulated miRNAs altered by bromelain in CaCO2 cells compared to in DLD-1 cells indicated that ACSL-4 is a key regulatory molecule.	Bromelain effectively suppresses Kras-mutant colorectal cancer by stimulating ferroptosis	2018	30460115
hsa-miR-17-5p	MIMAT0000070	miRNA	-	H.sapiens	Colorectal Cancer	CaCO2 cell line (up regulation)	miScript System (miRNA PCR Array miFinder)	Erastin	ACSL4	lipid ROS	elevated miR-19b-3p, -130a-3p, -150-5p, -144-3p, -16-5p, -7a-5p, and -17-5p in bromelain-treated CaCO2 cells compared to in DLD-1 cells potentially targeted ACSL-4 	Interactome analysis between these down-regulated gene and up-regulated miRNAs altered by bromelain in CaCO2 cells compared to in DLD-1 cells indicated that ACSL-4 is a key regulatory molecule.	Bromelain effectively suppresses Kras-mutant colorectal cancer by stimulating ferroptosis	2018	30460115