General Information of the Ferroptosis Regulator (ID: REG10331)
Regulator Name Cytoplasmic polyadenylation element-binding protein 1 (CPEB1)
Synonyms
CPEB
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Gene Name CPEB1
Gene ID 64506
Regulator Type Protein coding
Uniprot ID Q9BZB8
Sequence
MALSLEEEAGRIKDCWDNQEAPALSTCSNANIFRRINAILDNSLDFSRVCTTPINRGIHD
HLPDFQDSEETVTSRMLFPTSAQESSRGLPDANDLCLGLQSLSLTGWDRPWSTQDSDSSA
QSSTHSVLSMLHNPLGNVLGKPPLSFLPLDPLGSDLVDKFPAPSVRGSRLDTRPILDSRS
SSPSDSDTSGFSSGSDHLSDLISSLRISPPLPFLSLSGGGPRDPLKMGVGSRMDQEQAAL
AAVTPSPTSASKRWPGASVWPSWDLLEAPKDPFSIEREARLHRQAAAVNEATCTWSGQLP
PRNYKNPIYSCKVFLGGVPWDITEAGLVNTFRVFGSLSVEWPGKDGKHPRCPPKGNMPKG
YVYLVFELEKSVRSLLQACSHDPLSPDGLSEYYFKMSSRRMRCKEVQVIPWVLADSNFVR
SPSQRLDPSRTVFVGALHGMLNAEALAAILNDLFGGVVYAGIDTDKHKYPIGSGRVTFNN
QRSYLKAVSAAFVEIKTTKFTKKVQIDPYLEDSLCHICSSQPGPFFCRDQVCFKYFCRSC
WHWRHSMEGLRHHSPLMRNQKNRDSS

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Family RRM CPEB family
Function
Sequence-specific RNA-binding protein that regulates mRNA cytoplasmic polyadenylation and translation initiation during oocyte maturation, early development and at postsynapse sites of neurons. Binds to the cytoplasmic polyadenylation element (CPE), an uridine-rich sequence element (consensus sequence 5'-UUUUUAU-3') within the mRNA 3'- UTR. RNA binding results in a clear conformational change analogous to the Venus fly trap mechanism. In absence of phosphorylation and in association with TACC3 is also involved as a repressor of translation of CPE-containing mRNA; a repression that is relieved by phosphorylation or degradation. Involved in the transport of CPE-containing mRNA to dendrites; those mRNAs may be transported to dendrites in a translationally dormant form and translationally activated at synapses. Its interaction with APLP1 promotes local CPE-containing mRNA polyadenylation and translation activation. Induces the assembly of stress granules in the absence of stress. Required for cell cycle progression, specifically for prophase entry.

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HGNC ID
HGNC:21744
KEGG ID hsa:64506
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
CPEB1 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
Glutathione-specific gamma-glutamylcyclotransferase 1 (CHAC1) [Driver; Marker]
In total 1 item(s) under this target
Experiment 1 Reporting the Ferroptosis Target of This Regulator [1]
Target for Ferroptosis Marker/Driver
Responsed Disease Gastric cancer ICD-11: 2B72
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
AGS cells Gastric adenocarcinoma Homo sapiens CVCL_0139
SNU-1 cells Gastric adenocarcinoma Homo sapiens CVCL_0099
Hs746T cells Gastric adenocarcinoma Homo sapiens CVCL_0333
HGC-27 cells Gastric carcinoma Homo sapiens CVCL_1279
GES-1 cells Normal Homo sapiens CVCL_EQ22
In Vivo Model
Healthy male nude mice for 5 weeks were randomly divided into four groups, namely: A: Lv-NC + Vehicle group, B: Lv-NC + Erastin group, C: Lv-exCPEB1 + Vehicle group, and D: Lv-exCPEB1 + Erastin group. The living environment of nude mice in each group was 12 h light and 12 h dark, the temperature was 22 ± 1, the humidity was 45-55%. The model was established 1 week after adaptive feeding. GC cells (1 x 106) with stable overexpression of CPEB1 at the logarithmic growth stage were selected and injected subcutaneously in nude mice. When the tumor volume reached 100 mm3, nude mice in groups B and D were injected intraperitoneally with Erastin (30 mg/kg) twice a day (morning and night, respectively), and the tumor tissue diameter and volume were measured and calculated every 3 days after administration.

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Response regulation CPEB1 overexpression reduced the expression of twist1, an inhibitor of activating transcription factor 4 (ATF4), thereby activating the ATF4/ChaC Glutathione Specific Gamma-Glutamylcyclotransferase 1 (CHAC1) pathway (CHAC1, a molecule known to induce GSH degradation). Furthermore, re-expression of twist1 in gastric cancer cells impaired the effects of CPEB1 overexpression in presence of erastin.
Gastric cancer [ICD-11: 2B72]
In total 1 item(s) under this disease
Experiment 1 Reporting the Ferroptosis-centered Disease Response [1]
Target Regulator Cytoplasmic polyadenylation element-binding protein 1 (CPEB1) Protein coding
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Cell Process Cell ferroptosis
Cell proliferation
In Vitro Model
AGS cells Gastric adenocarcinoma Homo sapiens CVCL_0139
SNU-1 cells Gastric adenocarcinoma Homo sapiens CVCL_0099
Hs746T cells Gastric adenocarcinoma Homo sapiens CVCL_0333
HGC-27 cells Gastric carcinoma Homo sapiens CVCL_1279
GES-1 cells Normal Homo sapiens CVCL_EQ22
In Vivo Model
Healthy male nude mice for 5 weeks were randomly divided into four groups, namely: A: Lv-NC + Vehicle group, B: Lv-NC + Erastin group, C: Lv-exCPEB1 + Vehicle group, and D: Lv-exCPEB1 + Erastin group. The living environment of nude mice in each group was 12 h light and 12 h dark, the temperature was 22 ± 1, the humidity was 45-55%. The model was established 1 week after adaptive feeding. GC cells (1 x 106) with stable overexpression of CPEB1 at the logarithmic growth stage were selected and injected subcutaneously in nude mice. When the tumor volume reached 100 mm3, nude mice in groups B and D were injected intraperitoneally with Erastin (30 mg/kg) twice a day (morning and night, respectively), and the tumor tissue diameter and volume were measured and calculated every 3 days after administration.

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Response regulation CPEB1 overexpression reduced the expression of twist1, an inhibitor of activating transcription factor 4 (ATF4), thereby activating the ATF4/ChaC Glutathione Specific Gamma-Glutamylcyclotransferase 1 (CHAC1) pathway (CHAC1, a molecule known to induce GSH degradation). Furthermore, re-expression of twist1 in gastric cancer cells impaired the effects of CPEB1 overexpression in presence of erastin.
References
Ref 1 CPEB1 enhances erastin-induced ferroptosis in gastric cancer cells by suppressing twist1 expression. IUBMB Life. 2021 Sep;73(9):1180-1190. doi: 10.1002/iub.2525. Epub 2021 Jul 12.