DJ-1 promotes development of DEN-induced hepatocellular carcinoma and proliferation of liver cancer cells

Oncotarget. 2017 Jan 31;8(5):8499-8511. doi: 10.18632/oncotarget.14293.

Abstract

Chronic liver inflammation and injuries play a critical role in development of hepatocellular carcinoma (HCC). Parkinson disease (autosomal recessive, early onset) 7, encoding PARK7 protein (also called DJ-1), plays important roles in many carcinogenesis processes and is essential in modulating inflammation. However, whether DJ-1 is involved in HCC development remains largely unknown. To determine the effect of DJ-1 on HCC development, we accessed the correlation of hepatic DJ-1 expression with overall survival (OS) and TNM stage in 96 HCC patients and found a significant inverse correlation between DJ-1 expression and OS. By adopting a classic diethylnitrosamine (DEN)-induced murine HCC model, DJ-1 knockout (KO) mice displayed reduced tumorigenesis and cell proliferation, accompanied by decreased hepatic inflammation and IL-6/STAT3 activation. Furthermore, after an acute DEN challenge, DJ-1 KO mice showed significant decreases in liver injury, hepatocyte proliferation and DNA damage. In a human HCC cell line (MHCC-97L), cancer cell proliferation was induced by overexpression of DJ-1 and is related to oncogenic signaling of MAPKs and AKT. Induction of DJ-1 may serve as a novel regulator for HCC cell proliferation and HCC development possibly through enhanced MAPK signaling and inflammation.

Keywords: DJ-1; IL-6/STAT3; MHCC-97L; hepatocellular carcinoma.

MeSH terms

  • Animals
  • Carcinoma, Hepatocellular / enzymology*
  • Carcinoma, Hepatocellular / genetics
  • Carcinoma, Hepatocellular / pathology
  • Cell Line, Tumor
  • Cell Proliferation*
  • Diethylnitrosamine*
  • Genetic Predisposition to Disease
  • Humans
  • Interleukin-6 / metabolism
  • Liver Neoplasms / chemically induced
  • Liver Neoplasms / enzymology*
  • Liver Neoplasms / genetics
  • Liver Neoplasms / pathology
  • Male
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mitogen-Activated Protein Kinases / metabolism
  • Phenotype
  • Protein Deglycase DJ-1 / deficiency
  • Protein Deglycase DJ-1 / genetics
  • Protein Deglycase DJ-1 / metabolism*
  • Proto-Oncogene Proteins c-akt / metabolism
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction
  • Time Factors
  • Transfection

Substances

  • Interleukin-6
  • STAT3 Transcription Factor
  • Stat3 protein, mouse
  • interleukin-6, mouse
  • Diethylnitrosamine
  • Proto-Oncogene Proteins c-akt
  • Mitogen-Activated Protein Kinases
  • PARK7 protein, human
  • PARK7 protein, mouse
  • Protein Deglycase DJ-1