Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG30049)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
CBSLR
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]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Target for Ferroptosis | Driver | ||||
Responsed Disease | Gastric cancer | ICD-11: 2B72 | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Fatty acid metabolism | hsa01212 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
MKN45 cells | Gastric adenocarcinoma | Homo sapiens | CVCL_0434 | |
MKN-28 cells | Gastric epithelial carcinoma | Homo sapiens | CVCL_1416 | ||
In Vivo Model |
Female non-obese diabetic severe combined immune-deficient mice at 5 weeks of age were divided into indicated groups and injected subcutaneously at either side of flank area with indicated cell lines (1 x 106 cells) suspended in 0.1 ml phosphate-buffered saline (PBS). Tumor sizes in all groups were measured every 3 days using Vernier calipers and calculated using the following formula: (length x width2)/2. For the xenograft Cisplatin treatment assay, day 0 was designed when tumors reached around 50 mm3 in volume. DDP 7 mg/kg or carrier (PBS, 100 uL)) was injected intraperitoneally 1 time per week. 21 days after treatment, all mice were sacrificed and tumors were harvested and weighed. Representative images were presented, and all experiments were repeated at least 3 times.
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Response regulation | Schematic diagram showing that HIF-1 induces lncRNA-CBSLR to recruit YTHDF2 protein and CBS mRNA to form CBSLR/ YTHDF2/CBS complex, which in turn decreases CBS mRNA stability in an m6A dependent manner. The decreased CBS expression reduced methylation of ACSL4 protein, thus, the protein is degraded via the ubiquitination-proteasome pathway. Hypoxia inducible lncRNA-CBSLR modulates ferroptosis through m6A-YTHDF2-dependent modulation of CBS in gastric cancer. | ||||
Gastric cancer [ICD-11: 2B72]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | CBSLR (IncRNA) | lncRNA | |||
Pathway Response | Ferroptosis | hsa04216 | |||
Fatty acid metabolism | hsa01212 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
MKN45 cells | Gastric adenocarcinoma | Homo sapiens | CVCL_0434 | |
MKN-28 cells | Gastric epithelial carcinoma | Homo sapiens | CVCL_1416 | ||
In Vivo Model |
Female non-obese diabetic severe combined immune-deficient mice at 5 weeks of age were divided into indicated groups and injected subcutaneously at either side of flank area with indicated cell lines (1 x 106 cells) suspended in 0.1 ml phosphate-buffered saline (PBS). Tumor sizes in all groups were measured every 3 days using Vernier calipers and calculated using the following formula: (length x width2)/2. For the xenograft Cisplatin treatment assay, day 0 was designed when tumors reached around 50 mm3 in volume. DDP 7 mg/kg or carrier (PBS, 100 uL)) was injected intraperitoneally 1 time per week. 21 days after treatment, all mice were sacrificed and tumors were harvested and weighed. Representative images were presented, and all experiments were repeated at least 3 times.
Click to Show/Hide
|
||||
Response regulation | Schematic diagram showing that HIF-1 induces lncRNA-CBSLR to recruit YTHDF2 protein and CBS mRNA to form CBSLR/ YTHDF2/CBS complex, which in turn decreases CBS mRNA stability in an m6A dependent manner. The decreased CBS expression reduced methylation of ACSL4 protein, thus, the protein is degraded via the ubiquitination-proteasome pathway. Hypoxia inducible lncRNA-CBSLR modulates ferroptosis through m6A-YTHDF2-dependent modulation of CBS in gastric cancer. | ||||