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The AKT-independent MET-V-ATPase-MTOR axis suppresses liver cancer vaccination.


ABSTRACT: Despite recent progress in hepatitis treatment, there have been no significant advances in the development of liver cancer vaccines in recent years. In this study, we investigated the regulatory effect and potential mechanism of hepatocyte growth factor receptor (MET, also known as HGFR) on tumor vaccinations for liver cancer in mice. Herein, we demonstrate that MET expression is significantly associated with the immunogenicity of liver cancer in mice and humans, and that MET depletion dramatically enhances the protective efficacy of chemotherapy-based anti-liver cancer vaccination. Mechanistically, MET repressed liver cancer immunogenicity independent of the traditional PI3K-AKT cascade, and MET interacted with vacuolar ATP synthase (V-ATPase) and mediated the activation of mammalian target of rapamycin (MTOR), thus suppressing liver cancer immunogenicity. The efficacy of chemotherapy-based liver cancer vaccination was markedly enhanced by targeting the MET-V-ATPase-MTOR axis, highlighting a translational strategy for identifying MET-associated drug candidates for cancer prevention.

SUBMITTER: Huang X 

PROVIDER: S-EPMC7414041 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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The AKT-independent MET-V-ATPase-MTOR axis suppresses liver cancer vaccination.

Huang Xing X   Xu Xingyuan X   Wang Xun X   Tang Tianyu T   Li Enliang E   Zhang Xiaozhen X   Xu Jian J   Shen Hang H   Guo Chengxiang C   Xu Tao T   Ren Jianhong J   Bai Xueli X   Liang Tingbo T  

Signal transduction and targeted therapy 20200807 1


Despite recent progress in hepatitis treatment, there have been no significant advances in the development of liver cancer vaccines in recent years. In this study, we investigated the regulatory effect and potential mechanism of hepatocyte growth factor receptor (MET, also known as HGFR) on tumor vaccinations for liver cancer in mice. Herein, we demonstrate that MET expression is significantly associated with the immunogenicity of liver cancer in mice and humans, and that MET depletion dramatica  ...[more]

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