General Information of the m6A Target Gene (ID: M6ATAR00764)
Target Name Glucose-6-phosphate dehydrogenase (G6PD)
Synonyms
Glucose-6-phosphate 1-dehydrogenase; G6PD; EC 1.1.1.49
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Gene Name G6PD
Chromosomal Location Xq28
Family Glucose-6-phosphate dehydrogenase family
Function
Catalyzes the rate-limiting step of the oxidative pentose-phosphate pathway, which represents a route for the dissimilation of carbohydrates besides glycolysis. The main function of this enzyme is to provide reducing power (NADPH) and pentose phosphates for fatty acid and nucleic acid synthesis.
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Gene ID 2539
Uniprot ID
G6PD_HUMAN
HGNC ID
HGNC:4057
Ensembl Gene ID
ENSG00000160211.19
KEGG ID
hsa:2539
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).
Browse Regulator
Browse Disease
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
References
Ref 1 FTO promotes colorectal cancer progression and chemotherapy resistance via demethylating G6PD/PARP1. Clin Transl Med. 2022 Mar;12(3):e772. doi: 10.1002/ctm2.772.