Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG10463)
Regulator Name Ubiquitin-fold modifier 1 (UFM1)
Gene Name UFM1
Gene ID 51569
Regulator Type Protein coding
Uniprot ID P61960
Sequence
MSKVSFKITLTSDPRLPYKVLSVPESTPFTAVLKFAAEEFKVPAATSAIITNDGIGINPA
QTAGNVFLKHGSELRIIPRDRVGSC

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Family UFM1 family
Function
Ubiquitin-like modifier which can be covalently attached via an isopeptide bond to lysine residues of substrate proteins as a monomer or a lysine-linked polymer. The so-called ufmylation, requires the UFM1-activating E1 enzyme UBA5, the UFM1-conjugating E2 enzyme UFC1, and the UFM1-ligase E3 enzyme UFL1. Ufmylation is involved in reticulophagy (also called ER-phagy) induced in response to endoplasmic reticulum stress. Ufmylation of TRIP4 regulates nuclear receptors-mediated transcription.

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HGNC ID
HGNC:20597
KEGG ID hsa:51569
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
UFM1 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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Cystine/glutamate transporter (SLC7A11) [Driver; Suppressor]
 Target Info 
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Suppressor
Responsed Disease Breast cancer ICD-11: 2C60
 Disease Info 
Responsed Drug Metformin Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
 MCF-7 cells Breast carcinoma Homo sapiens CVCL_0031
T-47D cells Invasive breast carcinoma Homo sapiens CVCL_0553
HCC1937 cells Breast ductal carcinoma Homo sapiens CVCL_0290
Bcap37 cells Breast carcinoma Homo sapiens CVCL_0164
HBL-100 cells Normal Homo sapiens CVCL_4362
MDA-MB-231 cells Breast adenocarcinoma Homo sapiens CVCL_0062
BT-549 cells Invasive breast carcinoma Homo sapiens CVCL_1092
In Vivo Model
T47D xenografts were established in 5-week-old nude mice (Shanghai SLAC Laboratory Animal Corporation) by inoculating 1 x 107 cells mixed with Matrigel (BD Biosciences) at 1:1 ratio (volume) into the abdominal mammary fat pad. When the tumor reached 50-100 mm3, the mice were assigned randomly into different treatment groups (DMSO, Metformin, SAS, and Metformin + SAS groups). Metformin (200 mg/kg/day) was provided in drinking water. Sulfasalazine was dissolved in dimethyl sulfoxide (DMSO), diluted in PBS, and then intraperitoneally injected into mice at a dose of 250 mg/kg once a day.

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Response regulation Metformin reduces the protein stability of SLC7A11, which is a critical ferroptosis regulator, by inhibiting its UFMylation process. Furthermore, metformin combined with sulfasalazine, the system xc-inhibitor, can work in a synergistic manner to induce ferroptosis and inhibit the proliferation of breast cancer cells.
Breast cancer [ICD-11: 2C60]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Ubiquitin-fold modifier 1 (UFM1) Protein coding
 Regulator Info 
Responsed Drug Metformin Investigative
 Drug Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
 MCF-7 cells Breast carcinoma Homo sapiens CVCL_0031
T-47D cells Invasive breast carcinoma Homo sapiens CVCL_0553
HCC1937 cells Breast ductal carcinoma Homo sapiens CVCL_0290
Bcap37 cells Breast carcinoma Homo sapiens CVCL_0164
HBL-100 cells Normal Homo sapiens CVCL_4362
MDA-MB-231 cells Breast adenocarcinoma Homo sapiens CVCL_0062
BT-549 cells Invasive breast carcinoma Homo sapiens CVCL_1092
In Vivo Model
T47D xenografts were established in 5-week-old nude mice (Shanghai SLAC Laboratory Animal Corporation) by inoculating 1 x 107 cells mixed with Matrigel (BD Biosciences) at 1:1 ratio (volume) into the abdominal mammary fat pad. When the tumor reached 50-100 mm3, the mice were assigned randomly into different treatment groups (DMSO, Metformin, SAS, and Metformin + SAS groups). Metformin (200 mg/kg/day) was provided in drinking water. Sulfasalazine was dissolved in dimethyl sulfoxide (DMSO), diluted in PBS, and then intraperitoneally injected into mice at a dose of 250 mg/kg once a day.

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Response regulation Metformin reduces the protein stability of SLC7A11, which is a critical ferroptosis regulator, by inhibiting its UFMylation process. Furthermore, metformin combined with sulfasalazine, the system xc-inhibitor, can work in a synergistic manner to induce ferroptosis and inhibit the proliferation of breast cancer cells.
Metformin [Investigative]
 Drug Info 
In total 1 item(s) under this drug
Experiment 1 Reporting the Ferroptosis-centered Drug Response [1]
Drug for Ferroptosis Inducer
Response Target Cystine/glutamate transporter (SLC7A11) Driver; Suppressor
 Target Info 
Responsed Disease Breast cancer ICD-11: 2C60
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
 MCF-7 cells Breast carcinoma Homo sapiens CVCL_0031
T-47D cells Invasive breast carcinoma Homo sapiens CVCL_0553
HCC1937 cells Breast ductal carcinoma Homo sapiens CVCL_0290
Bcap37 cells Breast carcinoma Homo sapiens CVCL_0164
HBL-100 cells Normal Homo sapiens CVCL_4362
MDA-MB-231 cells Breast adenocarcinoma Homo sapiens CVCL_0062
BT-549 cells Invasive breast carcinoma Homo sapiens CVCL_1092
In Vivo Model
T47D xenografts were established in 5-week-old nude mice (Shanghai SLAC Laboratory Animal Corporation) by inoculating 1 x 107 cells mixed with Matrigel (BD Biosciences) at 1:1 ratio (volume) into the abdominal mammary fat pad. When the tumor reached 50-100 mm3, the mice were assigned randomly into different treatment groups (DMSO, Metformin, SAS, and Metformin + SAS groups). Metformin (200 mg/kg/day) was provided in drinking water. Sulfasalazine was dissolved in dimethyl sulfoxide (DMSO), diluted in PBS, and then intraperitoneally injected into mice at a dose of 250 mg/kg once a day.

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Response regulation Metformin reduces the protein stability of SLC7A11, which is a critical ferroptosis regulator, by inhibiting its UFMylation process. Furthermore, metformin combined with sulfasalazine, the system xc-inhibitor, can work in a synergistic manner to induce ferroptosis and inhibit the proliferation of breast cancer cells.
References
Ref 1 Metformin induces Ferroptosis by inhibiting UFMylation of SLC7A11 in breast cancer. J Exp Clin Cancer Res. 2021 Jun 23;40(1):206. doi: 10.1186/s13046-021-02012-7.