Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG10495)
Regulator Name Protein C-ets-1 (ETS1)
Synonyms
EWSR2; p54
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Gene Name ETS1
Gene ID 2113
Regulator Type Protein coding
Uniprot ID P14921
Sequence
MKAAVDLKPTLTIIKTEKVDLELFPSPDMECADVPLLTPSSKEMMSQALKATFSGFTKEQ
QRLGIPKDPRQWTETHVRDWVMWAVNEFSLKGVDFQKFCMNGAALCALGKDCFLELAPDF
VGDILWEHLEILQKEDVKPYQVNGVNPAYPESRYTSDYFISYGIEHAQCVPPSEFSEPSF
ITESYQTLHPISSEELLSLKYENDYPSVILRDPLQTDTLQNDYFAIKQEVVTPDNMCMGR
TSRGKLGGQDSFESIESYDSCDRLTQSWSSQSSFNSLQRVPSYDSFDSEDYPAALPNHKP
KGTFKDYVRDRADLNKDKPVIPAAALAGYTGSGPIQLWQFLLELLTDKSCQSFISWTGDG
WEFKLSDPDEVARRWGKRKNKPKMNYEKLSRGLRYYYDKNIIHKTAGKRYVYRFVCDLQS
LLGYTPEELHAMLDVKPDADE

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Family ETS family
Function
Transcription factor. Directly controls the expression of cytokine and chemokine genes in a wide variety of different cellular contexts. May control the differentiation, survival and proliferation of lymphoid cells. May also regulate angiogenesis through regulation of expression of genes controlling endothelial cell migration and invasion.; [Isoform Ets-1 p27]: Acts as a dominant-negative for isoform c-ETS-1A.

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HGNC ID
HGNC:3488
KEGG ID hsa:2113
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
ETS1 can regulate the following target(s), and cause disease/drug response(s). You can browse detail information of target(s) or disease/drug response(s).
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Long-chain-fatty-acid--CoA ligase 4 (ACSL4) [Driver]
 Target Info 
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Driver
Responsed Disease Hepatocellular carcinoma ICD-11: 2C12
 Disease Info 
Responsed Drug Sorafenib Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 MHCC97-L cells Hepatocellular carcinoma Homo sapiens CVCL_4973
PLC/PRF/5 cells Hepatocellular carcinoma Homo sapiens CVCL_0485
HEK293 FT cells Normal Homo sapiens CVCL_6911
In Vivo Model
Parental MHCC97L cells (2 x 106 cells/mouse) were subcutaneously injected into the 4-to-5-week-old NOD-SCID mice. When the tumours reached a volume of around 50-100 mm3 (calculated by the formula 4/3(D/2)(d/2)2, where D and d represent the minor and major axis of the tumour, respectively), the maximum tolerated dose of sorafenib (50 mg/kg) was given to the mice by oral gavage daily until the drug resistance occurred, denoted as the drug resistant group. For the control, the wild type group was treated with the vehicle (0.5% CMC-Na). The tumour size and body weight were measured every 3 days.

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Response regulation Sorafenib treatment triggered ferroptosis via lipid ROS production and chelatable iron accumulation. The ETS1 upregulated by sorafenib was a key transcription factor of miR-23a-3p that directly enhanced miR-23a-3p expression. MiR-23a-3p recognized and bound to ACSL4 3UTR to limit lipid ROS production, thus attenuating sorafenib-induced ferroptotic cell death in hepatocellular carcinoma.
Hepatocellular carcinoma [ICD-11: 2C12]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Protein C-ets-1 (ETS1) Protein coding
 Regulator Info 
Responsed Drug Sorafenib Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 MHCC97-L cells Hepatocellular carcinoma Homo sapiens CVCL_4973
PLC/PRF/5 cells Hepatocellular carcinoma Homo sapiens CVCL_0485
HEK293 FT cells Normal Homo sapiens CVCL_6911
In Vivo Model
Parental MHCC97L cells (2 x 106 cells/mouse) were subcutaneously injected into the 4-to-5-week-old NOD-SCID mice. When the tumours reached a volume of around 50-100 mm3 (calculated by the formula 4/3(D/2)(d/2)2, where D and d represent the minor and major axis of the tumour, respectively), the maximum tolerated dose of sorafenib (50 mg/kg) was given to the mice by oral gavage daily until the drug resistance occurred, denoted as the drug resistant group. For the control, the wild type group was treated with the vehicle (0.5% CMC-Na). The tumour size and body weight were measured every 3 days.

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Response regulation Sorafenib treatment triggered ferroptosis via lipid ROS production and chelatable iron accumulation. The ETS1 upregulated by sorafenib was a key transcription factor of miR-23a-3p that directly enhanced miR-23a-3p expression. MiR-23a-3p recognized and bound to ACSL4 3UTR to limit lipid ROS production, thus attenuating sorafenib-induced ferroptotic cell death in hepatocellular carcinoma.
Sorafenib [Investigative]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response [1]
Drug for Ferroptosis Suppressor
Response Target Long-chain-fatty-acid--CoA ligase 4 (ACSL4) Driver
 Target Info 
Responsed Disease Hepatocellular carcinoma ICD-11: 2C12
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
In Vitro Model
 MHCC97-L cells Hepatocellular carcinoma Homo sapiens CVCL_4973
PLC/PRF/5 cells Hepatocellular carcinoma Homo sapiens CVCL_0485
HEK293 FT cells Normal Homo sapiens CVCL_6911
In Vivo Model
Parental MHCC97L cells (2 x 106 cells/mouse) were subcutaneously injected into the 4-to-5-week-old NOD-SCID mice. When the tumours reached a volume of around 50-100 mm3 (calculated by the formula 4/3(D/2)(d/2)2, where D and d represent the minor and major axis of the tumour, respectively), the maximum tolerated dose of sorafenib (50 mg/kg) was given to the mice by oral gavage daily until the drug resistance occurred, denoted as the drug resistant group. For the control, the wild type group was treated with the vehicle (0.5% CMC-Na). The tumour size and body weight were measured every 3 days.

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Response regulation Sorafenib treatment triggered ferroptosis via lipid ROS production and chelatable iron accumulation. The ETS1 upregulated by sorafenib was a key transcription factor of miR-23a-3p that directly enhanced miR-23a-3p expression. MiR-23a-3p recognized and bound to ACSL4 3UTR to limit lipid ROS production, thus attenuating sorafenib-induced ferroptotic cell death in hepatocellular carcinoma.
References
Ref 1 Epigenetic regulation of ferroptosis via ETS1/miR-23a-3p/ACSL4 axis mediates sorafenib resistance in human hepatocellular carcinoma. J Exp Clin Cancer Res. 2022 Jan 3;41(1):3. doi: 10.1186/s13046-021-02208-x.