Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG30067)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
LINC01004
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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Unspecific Target [Unspecific Target]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Responsed Disease | Oesophageal cancer | ICD-11: 2B70 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
TE-1 cells | Esophageal squamous cell carcinoma | Homo sapiens | CVCL_1759 | |
KYSE30 cells | Esophageal squamous cell carcinoma | Homo sapiens | CVCL_1351 | ||
In Vivo Model |
A total of 128 immune active female C57BL/6 mice (6 weeks old) were procured from SLAC Laboratory Animal Co., Ltd. (Shanghai, China). ESCC cells (TE-1 and KYSE-30) resuspended in PBS were mixed with Matrigel and subcutaneously injected into the mice (1 x 106 cells per mouse) at the right flank to induce subcutaneous tumors. When the tumor size reached around 150 mm3, the tumor site was locally exposed to irradiation (2 Gy/d for consecutive 4 d). For antibody injection, the mice were injected with IgG or Anti-SIGECE on day 1, 7, or 14 after the first irradiation exposure. After 28 d, the mice were euthanized via overdosed barbiturate (150 mg/kg). The subcutaneous tumors were collected for IHC. Another group of ESCC cells were injected into mice via tail vein (2 x 106 cells per mouse).
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Response regulation | LINC01004 recruited Spi-1 proto-oncogene (SPI1) in nucleus of TAMs to induce transcriptional activation of SIGLEC9. SIGLEC9 interacted with mucin 1 (MUC1). MUC1 overexpression in esophageal squamous cell carcinoma (ESCC) induced M2 skewing of TAMs, enhanced radioresistance and immunosuppression, and promoted nuclear translocation of -catenin to suppress radiotherapy-induced ferroptosis of ESCC cells. | ||||
Oesophageal cancer [ICD-11: 2B70]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | LINC01004 (IncRNA) | lncRNA | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
Cell proliferation | |||||
In Vitro Model |
TE-1 cells | Esophageal squamous cell carcinoma | Homo sapiens | CVCL_1759 | |
KYSE30 cells | Esophageal squamous cell carcinoma | Homo sapiens | CVCL_1351 | ||
In Vivo Model |
A total of 128 immune active female C57BL/6 mice (6 weeks old) were procured from SLAC Laboratory Animal Co., Ltd. (Shanghai, China). ESCC cells (TE-1 and KYSE-30) resuspended in PBS were mixed with Matrigel and subcutaneously injected into the mice (1 x 106 cells per mouse) at the right flank to induce subcutaneous tumors. When the tumor size reached around 150 mm3, the tumor site was locally exposed to irradiation (2 Gy/d for consecutive 4 d). For antibody injection, the mice were injected with IgG or Anti-SIGECE on day 1, 7, or 14 after the first irradiation exposure. After 28 d, the mice were euthanized via overdosed barbiturate (150 mg/kg). The subcutaneous tumors were collected for IHC. Another group of ESCC cells were injected into mice via tail vein (2 x 106 cells per mouse).
Click to Show/Hide
|
||||
Response regulation | LINC01004 recruited Spi-1 proto-oncogene (SPI1) in nucleus of TAMs to induce transcriptional activation of SIGLEC9. SIGLEC9 interacted with mucin 1 (MUC1). MUC1 overexpression in esophageal squamous cell carcinoma (ESCC) induced M2 skewing of TAMs, enhanced radioresistance and immunosuppression, and promoted nuclear translocation of -catenin to suppress radiotherapy-induced ferroptosis of ESCC cells. | ||||
References