Open AccessStomach-specific c-Myc overexpression drives gastric adenoma in mice via AKT/mTOR signaling
Author(s) -
Jing Liu,
Wenlong Feng,
Min Liu,
Hanyu Rao,
Xiaoxue Li,
Yan Teng,
Xiao Yang,
Jin Xu,
WeiQiang Gao,
Li Li
Publication year - 2020
Publication title -
bosnian journal of basic medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 25
eISSN - 1840-4812
pISSN - 1512-8601
DOI - 10.17305/bjbms.2020.4978
Subject(s) - pi3k/akt/mtor pathway , protein kinase b , cancer research , carcinogenesis , oncogene , cancer , medicine , stomach , genetically modified mouse , rptor , transgene , signal transduction , biology , cell cycle , microbiology and biotechnology , gene , biochemistry
Gastric cancer (GC) is one of the most common malignant cancers in the world. c-Myc, a well-known oncogene, is commonly amplified in many cancers, including gastric cancer. However, it is still not completely understood how c-Myc functions in GC. Here, we generated a stomach-specific c-Myc transgenic mouse model to investigate its role in GC. We found that overexpression of c-Myc in Atp4b+ gastric parietal cells could induce gastric adenoma in mice. Mechanistically, c-Myc promoted tumorigenesis via the AKT/mTOR pathway. Furthermore, AKT inhibitor (MK-2206) or mTOR inhibitor (Rapamycin) inhibited the proliferation of c-Myc overexpressing gastric cancer cell lines. Thus, our findings highlight that gastric tumorigenesis can be induced by c-Myc overexpression through activation of the AKT/mTOR pathway.