m6A Target Gene Information
General Information of the m6A Target Gene (ID: M6ATAR00764)
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
G6PD
can be regulated by the following regulator(s), and cause disease/drug response(s). You can browse detail information of regulator(s) or disease/drug response(s).
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Fat mass and obesity-associated protein (FTO) [ERASER]
In total 1 item(s) under this regulator | ||||
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [1] | |||
Response Summary | Targeting FTO significantly suppresses cancer cell growth and enhances chemotherapy sensitivity, which not only mediating the balance of intracellular ROS by regulating Glucose-6-phosphate dehydrogenase (G6PD) expression, but also maintaining genome instability by regulating PARP1 expression. These findings shed light on new molecular mechanisms of CRC development and treatments mediated by m6A modification. | |||
Target Regulation | Up regulation | |||
Responsed Disease | Colorectal cancer | ICD-11: 2B91 | ||
Pathway Response | Glutathione metabolism | hsa00480 | ||
In-vitro Model | LoVo | Colon adenocarcinoma | Homo sapiens | CVCL_0399 |
HCT 116 | Colon carcinoma | Homo sapiens | CVCL_0291 | |
HCT 8 | Colon adenocarcinoma | Homo sapiens | CVCL_2478 | |
SW620 | Colon adenocarcinoma | Homo sapiens | CVCL_0547 | |
In-vivo Model | For CDX model, nude mice (female, 4-6-week-old) were subcutaneously injected with 5 × 106 HCT116 cells on the both flank. For PDX model, the patient tumors were divided into small pieces and then inoculated on both flank of nude mice. For knockdown FTO mice model, FTO mice model, two weeks after inoculation, the shFTO#3 lenti-virus injected into the tumor for three consecutive days. For combined medication mice model, intraperitoneal injection of Rhein and Olaparib was started one week after inoculation | |||
Colorectal cancer [ICD-11: 2B91]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the m6A-centered Disease Response | [1] | |||
Response Summary | Targeting FTO significantly suppresses cancer cell growth and enhances chemotherapy sensitivity, which not only mediating the balance of intracellular ROS by regulating Glucose-6-phosphate dehydrogenase (G6PD) expression, but also maintaining genome instability by regulating PARP1 expression. These findings shed light on new molecular mechanisms of CRC development and treatments mediated by m6A modification. | |||
Responsed Disease | Colorectal cancer [ICD-11: 2B91] | |||
Target Regulator | Fat mass and obesity-associated protein (FTO) | ERASER | ||
Target Regulation | Up regulation | |||
Pathway Response | Glutathione metabolism | hsa00480 | ||
In-vitro Model | LoVo | Colon adenocarcinoma | Homo sapiens | CVCL_0399 |
HCT 116 | Colon carcinoma | Homo sapiens | CVCL_0291 | |
HCT 8 | Colon adenocarcinoma | Homo sapiens | CVCL_2478 | |
SW620 | Colon adenocarcinoma | Homo sapiens | CVCL_0547 | |
In-vivo Model | For CDX model, nude mice (female, 4-6-week-old) were subcutaneously injected with 5 × 106 HCT116 cells on the both flank. For PDX model, the patient tumors were divided into small pieces and then inoculated on both flank of nude mice. For knockdown FTO mice model, FTO mice model, two weeks after inoculation, the shFTO#3 lenti-virus injected into the tumor for three consecutive days. For combined medication mice model, intraperitoneal injection of Rhein and Olaparib was started one week after inoculation | |||