m6A Target Gene Information

General Information of the m6A Target Gene (ID: M6ATAR00005)
Target Name Mammalian target of rapamycin complex 2 (mTORC2)
Gene Name mTORC2
Uniprot ID
SIN1_HUMAN, LST8_HUMAN, MTOR_HUMAN, PRR5_HUMAN, RICTR_HUMAN
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
mTORC2 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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Methyltransferase-like 14 (METTL14) [WRITER]
 Regulator Info 
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary About 70% of endometrial tumours exhibit reductions in m6A methylation that are probably due to either this METTL14 mutation or reduced expression of METTL3. Reductions in m6A methylation lead to decreased expression of the negative AKT regulator PHLPP2 and increased expression of the positive AKT regulator Mammalian target of rapamycin complex 2 (mTORC2). these results reveal reduced m6A mRNA methylation as an oncogenic mechanism in endometrial cancer and identify m6A methylation as a regulator of AKT signalling.
Target Regulation Down regulation
Responsed Disease Endometrial cancer ICD-11: 2C76
 Disease Info 
In-vitro Model HEC-1-A Endometrial adenocarcinoma Homo sapiens CVCL_0293
In-vivo Model 4×106 HEC-1-A endometrial cancer cells (shCtrl, shMETTL3, wild-type, METTL14+/-, or METTL14+/- rescued with wild-type or mutant METTL14) were injected intraperitoneally into 5 week old female athymic nude mice (Foxn1nu, Harlan; n=10 per group).
Methyltransferase-like 3 (METTL3) [WRITER]
 Regulator Info 
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary About 70% of endometrial tumours exhibit reductions in m6A methylation that are probably due to either this METTL14 mutation or reduced expression of METTL3. Reductions in m6A methylation lead to decreased expression of the negative AKT regulator PHLPP2 and increased expression of the positive AKT regulator Mammalian target of rapamycin complex 2 (mTORC2). these results reveal reduced m6A mRNA methylation as an oncogenic mechanism in endometrial cancer and identify m6A methylation as a regulator of AKT signalling.
Target Regulation Down regulation
Responsed Disease Endometrial cancer ICD-11: 2C76
 Disease Info 
Cell Process Cell proliferation and tumorigenicity
In-vitro Model HEC-1-A Endometrial adenocarcinoma Homo sapiens CVCL_0293
RL95-2 Endometrial adenosquamous carcinoma Homo sapiens CVCL_0505
T HESCs Normal Homo sapiens CVCL_C464
In-vivo Model 4×106 HEC-1-A endometrial cancer cells (shCtrl, shMETTL3, wild-type, METTL14+/-, or METTL14+/- rescued with wild-type or mutant METTL14) were injected intraperitoneally into 5 week old female athymic nude mice (Foxn1nu, Harlan; n=10 per group).
Endometrial cancer [ICD-11: 2C76]
 Disease Info 
In total 2 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary About 70% of endometrial tumours exhibit reductions in m6A methylation that are probably due to either this METTL14 mutation or reduced expression of METTL3. Reductions in m6A methylation lead to decreased expression of the negative AKT regulator PHLPP2 and increased expression of the positive AKT regulator Mammalian target of rapamycin complex 2 (mTORC2). these results reveal reduced m6A mRNA methylation as an oncogenic mechanism in endometrial cancer and identify m6A methylation as a regulator of AKT signalling.
Responsed Disease Endometrial cancer [ICD-11: 2C76]
Target Regulator Methyltransferase-like 14 (METTL14) WRITER
 Regulator Info 
Target Regulation Down regulation
In-vitro Model HEC-1-A Endometrial adenocarcinoma Homo sapiens CVCL_0293
In-vivo Model 4×106 HEC-1-A endometrial cancer cells (shCtrl, shMETTL3, wild-type, METTL14+/-, or METTL14+/- rescued with wild-type or mutant METTL14) were injected intraperitoneally into 5 week old female athymic nude mice (Foxn1nu, Harlan; n=10 per group).
Experiment 2 Reporting the m6A-centered Disease Response [1]
Response Summary About 70% of endometrial tumours exhibit reductions in m6A methylation that are probably due to either this METTL14 mutation or reduced expression of METTL3. Reductions in m6A methylation lead to decreased expression of the negative AKT regulator PHLPP2 and increased expression of the positive AKT regulator Mammalian target of rapamycin complex 2 (mTORC2). these results reveal reduced m6A mRNA methylation as an oncogenic mechanism in endometrial cancer and identify m6A methylation as a regulator of AKT signalling.
Responsed Disease Endometrial cancer [ICD-11: 2C76]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Down regulation
Cell Process Cell proliferation and tumorigenicity
In-vitro Model HEC-1-A Endometrial adenocarcinoma Homo sapiens CVCL_0293
RL95-2 Endometrial adenosquamous carcinoma Homo sapiens CVCL_0505
T HESCs Normal Homo sapiens CVCL_C464
In-vivo Model 4×106 HEC-1-A endometrial cancer cells (shCtrl, shMETTL3, wild-type, METTL14+/-, or METTL14+/- rescued with wild-type or mutant METTL14) were injected intraperitoneally into 5 week old female athymic nude mice (Foxn1nu, Harlan; n=10 per group).
References
Ref 1 m(6)A mRNA methylation regulates AKT activity to promote the proliferation and tumorigenicity of endometrial cancer. Nat Cell Biol. 2018 Sep;20(9):1074-1083. doi: 10.1038/s41556-018-0174-4. Epub 2018 Aug 27.