The molecular mechanism on the association of diabetes mellitus with hepatocellular carcinoma

Authors

  • Wanming Zheng Department of General Surgery, Chongqing Traditional Chinese Medicine Hospital of Yubei District, Chongqing, China
  • Minghua Deng Department of Hepatobiliary Surgery, Yubei District People's Hospital of Chongqing, Chongqing, China
  • Jianping Gong Department of Hepatobiliary Surgery, Second affiliated Hospital of Chongqing Medical University, Chongqing, China

DOI:

https://doi.org/10.18203/2349-2902.isj20205921

Keywords:

Diabetes mellitus, Hepatocellular carcinoma, Insulin-like growth factor, Toll-like receptor 4, NCOA5

Abstract

Many studies have shown a complex link between diabetes mellitus and hepatocellular carcinoma. Diabetes mellitus is an independent risk factor for the development of hepatocellular carcinoma (HCC), and increase both the morbidity and mortality of HCC in many ways, including insulin resistance, hyperglycemia, hyperinsulinemia, inflammation and metabolic dysfunction. Insulin-like growth factor (IGF) axis, WNT/β-catenin pathway and glycogen synthase kinase 3 (GSK3) were dysregulated in liver metabolism of diabetics and cause damage to hepatocytes, which would increase risk for HCC. The toll-like receptor 4 (TLR4) could affect the two diseases through the NF-κB pathway, when the liver is under metabolic dysfunction. Moreover, single nucleotide variation (SNV) (T445A) in NCOA5 is a confirmed pathogenic in these HCC patients with diabetes mellitus.

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Published

2020-12-28

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Section

Review Articles