Stomach-specific c-Myc overexpression drives gastric adenoma in mice through AKT/mammalian target of rapamycin signaling

  • Bosn J Basic Med Sci. 2021 Aug 1;21(4):434-446. doi: 10.17305/bjbms.2020.4978.
Jing Liu  1 ,  Wenxin Feng  1 ,  Min Liu  1 ,  Hanyu Rao  1 ,  Xiaoxue Li  1 ,  Yan Teng  2 ,  Xiao Yang  2 ,  Jin Xu  3 ,  Weiqiang Gao  1 ,  Li Li  1
Affiliations
  • 1. State Key Laboratory of Oncogenes and Related Genes, Renji Med-X Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China; School of Biomedical Engineering and Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China.
  • 2. State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences, Beijing Institute of Lifeomics, Beijing, China.
  • 3. School of Biomedical Engineering and Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China.
PMID: 33259779 DOI: 10.17305/bjbms.2020.4978
Abstract

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.

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