Ferroptosis Regulator Information

General Information of the Ferroptosis Regulator (ID: REG10007)
Regulator Name Membrane-associated progesterone receptor component 1 (PGRMC1)
Synonyms
Dap1
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Gene Name PGRMC1
Gene ID 10857
Regulator Type Protein coding
Uniprot ID O00264
Sequence
MAAEDVVATGADPSDLESGGLLHEIFTSPLNLLLLGLCIFLLYKIVRGDQPAASGDSDDD
EPPPLPRLKRRDFTPAELRRFDGVQDPRILMAINGKVFDVTKGRKFYGPEGPYGVFAGRD
ASRGLATFCLDKEALKDEYDDLSDLTAAQQETLSDWESQFTFKYHHVGKLLKEGEEPTVY
SDEEEPKDESARKND

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Family Cytochrome b5 family
Function
Component of a progesterone-binding protein complex. Binds progesterone. Has many reported cellular functions (heme homeostasis, interaction with CYPs). Required for the maintenance of uterine histoarchitecture and normal female reproductive lifespan. Intracellular heme chaperone. Regulates heme synthesis via interactions with FECH and acts as a heme donor for at least some hemoproteins.

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HGNC ID
HGNC:16090
KEGG ID hsa:10857
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
PGRMC1 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).
Browse Target
Browse Disease
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 Head neck squamous cell carcinoma ICD-11: 2D60
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model
 NH-3 cells Tongue squamous cell carcinoma Homo sapiens CVCL_8126
HN4 cells Clear cell renal cell carcinoma Homo sapiens CVCL_IS30
In Vivo Model
Six-week-old athymic BALB/c male nude mice (nu/nu) were purchased from OrientBio (Seoul, Republic of Korea). HN4 cells with transfection of PGRMC1 overexpression or control vector and HN4PCC with shPGRMC1 or control vector were subcutaneously injected into the bilateral flank of nude mice. When gross nodules were detected in tumor implants, mice were subjected to different treatments: vehicle or sulfasalazine (250 mg/kg daily per intraperitoneal route).

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Response regulation GRMC1-dependent lipophagy promotes ferroptosis in paclitaxel-tolerant persister cancer cells. PGRMC1 expression increased FAO and ferroptosis sensitivity from in vivo mice experiments. And PGRMC1 promotes ferroptosis by xCT (SLC7A11) inhibition in head and neck cancer (HNC) cells.
Head neck squamous cell carcinoma [ICD-11: 2D60]
 Disease Info 
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Membrane-associated progesterone receptor component 1 (PGRMC1) Protein coding
 Regulator Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell autophagy
In Vitro Model
 NH-3 cells Tongue squamous cell carcinoma Homo sapiens CVCL_8126
HN4 cells Clear cell renal cell carcinoma Homo sapiens CVCL_IS30
In Vivo Model
Six-week-old athymic BALB/c male nude mice (nu/nu) were purchased from OrientBio (Seoul, Republic of Korea). HN4 cells with transfection of PGRMC1 overexpression or control vector and HN4PCC with shPGRMC1 or control vector were subcutaneously injected into the bilateral flank of nude mice. When gross nodules were detected in tumor implants, mice were subjected to different treatments: vehicle or sulfasalazine (250 mg/kg daily per intraperitoneal route).

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Response regulation GRMC1-dependent lipophagy promotes ferroptosis in paclitaxel-tolerant persister cancer cells. PGRMC1 expression increased FAO and ferroptosis sensitivity from in vivo mice experiments. And PGRMC1 promotes ferroptosis by xCT (SLC7A11) inhibition in head and neck cancer (HNC) cells.
References
Ref 1 PGRMC1-dependent lipophagy promotes ferroptosis in paclitaxel-tolerant persister cancer cells. J Exp Clin Cancer Res. 2021 Nov 8;40(1):350. doi: 10.1186/s13046-021-02168-2.