General Information of the Ferroptosis Regulator (ID: REG30049)
Regulator Name CBSLR (IncRNA)
Synonyms
CBSLR
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Gene Name CBSLR
Gene ID 124904470
Regulator Type lncRNA
Ensembl ID .
HGNC ID
HGNC:55459
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.
References
Ref 1 Hypoxia inducible lncRNA-CBSLR modulates ferroptosis through m6A-YTHDF2-dependent modulation of CBS in gastric cancer. J Adv Res. 2021 Oct 5;37:91-106. doi: 10.1016/j.jare.2021.10.001. eCollection 2022 Mar.