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10.3390/cancers8080076

http://scihub22266oqcxt.onion/10.3390/cancers8080076
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C4999785!4999785!27556491
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suck abstract from ncbi


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pmid27556491      Cancers+(Basel) 2016 ; 8 (8): ä
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  • Epigenetic Activation of Wnt/?-Catenin Signaling in NAFLD-Associated Hepatocarcinogenesis #MMPMID27556491
  • Tian Y; Mok MT; Yang P; Cheng AS
  • Cancers (Basel) 2016[Aug]; 8 (8): ä PMID27556491show ga
  • Non-alcoholic fatty liver disease (NAFLD), characterized by fat accumulation in liver, is closely associated with central obesity, over-nutrition and other features of metabolic syndrome, which elevate the risk of developing hepatocellular carcinoma (HCC). The Wnt/?-catenin signaling pathway plays a significant role in the physiology and pathology of liver. Up to half of HCC patients have activation of Wnt/?-catenin signaling. However, the mutation frequencies of CTNNB1 (encoding ?-catenin protein) or other antagonists targeting Wnt/?-catenin signaling are low in HCC patients, suggesting that genetic mutations are not the major factor driving abnormal ?-catenin activities in HCC. Emerging evidence has demonstrated that obesity-induced metabolic pathways can deregulate chromatin modifiers such as histone deacetylase 8 to trigger undesired global epigenetic changes, thereby modifying gene expression program which contributes to oncogenic signaling. This review focuses on the aberrant epigenetic activation of Wnt/?-catenin in the development of NAFLD-associated HCC. A deeper understanding of the molecular mechanisms underlying such deregulation may shed light on the identification of novel druggable epigenetic targets for the prevention and/or treatment of HCC in obese and diabetic patients.
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