Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10331)
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.
Click to Show/Hide
|
||||
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.
Click to Show/Hide
|
||||
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. | ||||