Chronic inflammation contributes to the development of hepatocellular carcinoma by decreasing miR-122 levels

Oncotarget. 2016 Mar 29;7(13):17021-34. doi: 10.18632/oncotarget.7740.

Abstract

Persistent inflammation in chronic hepatitis plays a major role in the development of hepatocellular carcinoma (HCC). In this study, the major inflammatory cytokines expressed in chronic hepatitis, IL-6 and TNF-α, induced a marked decrease in microRNA-122 (miR-122) levels, and miR-122 expression was downregulated in the livers of chronic hepatitis B (CHB) patients. The decrease of miR-122 caused upregulation of the proinflammatory chemokine CCL2. IL-6 and TNF-α suppressed miR-122 both by directly downregulating the transcription factor C/EBPα and indirectly upregulating c-myc, which blocks C/EBPα-mediated miR-122 transcription. In addition, IL-6 and TNF-α levels were elevated and miR-122 levels were decreased in mouse and rat models of diethylnitrosamine (DEN)-induced HCC. Restoration of miR-122 levels through delivery of agomir-122 suppressed DEN-induced hepatocarcinogenesis in mice. Our results show that inflammation-induced miR-122 downregulation in hepatitis contributes to carcinogenesis and suggest that increasing miR-122 may be an effective strategy for preventing HCC development in CHB patients.

Keywords: C/EBPα; IL-6; TNF-α; c-myc; miR-122.

MeSH terms

  • Animals
  • Carcinogenesis / genetics
  • Carcinoma, Hepatocellular / etiology
  • Carcinoma, Hepatocellular / pathology*
  • Gene Expression Regulation, Neoplastic / physiology*
  • Hepatitis B, Chronic / complications
  • Humans
  • Inflammation / complications
  • Inflammation / pathology*
  • Liver Neoplasms / etiology
  • Liver Neoplasms / pathology*
  • Mice
  • Mice, Inbred C57BL
  • MicroRNAs / biosynthesis*
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction / physiology

Substances

  • MIRN122 microRNA, human
  • MicroRNAs