Nature Communications (Dec 2018)
An inflammatory-CCRK circuitry drives mTORC1-dependent metabolic and immunosuppressive reprogramming in obesity-associated hepatocellular carcinoma
- 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
Affiliations
- Hanyong Sun
- Department of Medicine and Therapeutics, The Chinese University of Hong Kong
- Weiqin Yang
- School of Biomedical Sciences, The Chinese University of Hong Kong
- Yuan Tian
- Department of Medicine and Therapeutics, The Chinese University of Hong Kong
- Xuezhen Zeng
- School of Biomedical Sciences, The Chinese University of Hong Kong
- Jingying Zhou
- School of Biomedical Sciences, The Chinese University of Hong Kong
- Myth T. S. Mok
- School of Biomedical Sciences, The Chinese University of Hong Kong
- Wenshu Tang
- School of Biomedical Sciences, The Chinese University of Hong Kong
- Yu Feng
- School of Biomedical Sciences, The Chinese University of Hong Kong
- Liangliang Xu
- School of Biomedical Sciences, The Chinese University of Hong Kong
- Anthony W. H. Chan
- Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong
- Joanna H. Tong
- Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong
- Yue-Sun Cheung
- Department of Surgery, The Chinese University of Hong Kong
- Paul B. S. Lai
- Department of Surgery, The Chinese University of Hong Kong
- Hector K. S. Wang
- Division of Life Science, The Hong Kong University of Science and Technology
- Shun-Wa Tsang
- Division of Life Science, The Hong Kong University of Science and Technology
- King-Lau Chow
- Division of Life Science, The Hong Kong University of Science and Technology
- Mengying Hu
- Division of Pharmacoengineering and Molecular Pharmaceutics, Eshelman School of Pharmacy, University of North Carolina at Chapel Hill
- Rihe Liu
- Division of Chemical Biology and Medicinal Chemistry, Eshelman School of Pharmacy and Carolina Center for Genome Sciences, University of North Carolina at Chapel Hill
- Leaf Huang
- Division of Pharmacoengineering and Molecular Pharmaceutics, Eshelman School of Pharmacy, University of North Carolina at Chapel Hill
- Bing Yang
- Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences
- Pengyuan Yang
- Key Laboratory of Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences
- Ka-Fai To
- Department of Anatomical and Cellular Pathology, The Chinese University of Hong Kong
- Joseph J. Y. Sung
- Department of Medicine and Therapeutics, The Chinese University of Hong Kong
- Grace L. H. Wong
- Department of Medicine and Therapeutics, The Chinese University of Hong Kong
- Vincent W. S. Wong
- Department of Medicine and Therapeutics, The Chinese University of Hong Kong
- Alfred S. L. Cheng
- School of Biomedical Sciences, The Chinese University of Hong Kong
- DOI
- https://doi.org/10.1038/s41467-018-07402-8
- Journal volume & issue
-
Vol. 9,
no. 1
pp. 1 – 16
Abstract
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.
