An inflammatory-CCRK circuitry drives mTORC1-dependent metabolic and immunosuppressive reprogramming in obesity-associated hepatocellular carcinoma

An inflammatory-CCRK circuitry drives mTORC1-dependent metabolic and immunosuppressive reprogramming in obesity-associated hepatocellular carcinoma

Obesity increases the risk of hepatocellular carcinoma (HCC) especially in men. Here the authors find a potential mechanistic explanation by showing that, in mice, obesity-induced STAT3 cooperates with the androgen receptor to activate the mTORC pathway through up regulation of CCRK, resulting in he...

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Autores principales: Hanyong Sun, Weiqin Yang, Yuan Tian, Xuezhen Zeng, Jingying Zhou, Myth T. S. Mok, Wenshu Tang, Yu Feng, Liangliang Xu, Anthony W. H. Chan, Joanna H. Tong, Yue-Sun Cheung, Paul B. S. Lai, Hector K. S. Wang, Shun-Wa Tsang, King-Lau Chow, Mengying Hu, Rihe Liu, Leaf Huang, Bing Yang, Pengyuan Yang, Ka-Fai To, Joseph J. Y. Sung, Grace L. H. Wong, Vincent W. S. Wong, Alfred S. L. Cheng
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2018
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Acceso en línea:https://doaj.org/article/6dd5d597aab145d5bf368e0227da0aaf
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Sumario:Obesity increases the risk of hepatocellular carcinoma (HCC) especially in men. Here the authors find a potential mechanistic explanation by showing that, in mice, obesity-induced STAT3 cooperates with the androgen receptor to activate the mTORC pathway through up regulation of CCRK, resulting in hepatic steatosis worsening and HCC development via metabolic and immune reprogramming.

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