2-Amino-3-methylimidazo[4,5-f]quinoline (IQ) promotes mouse hepatocarcinogenesis by activating transforming growth factor-β and Wnt/β-catenin signaling pathways

Toxicol Sci. 2012 Feb;125(2):392-400. doi: 10.1093/toxsci/kfr314. Epub 2011 Nov 17.

Abstract

The purposes of the present study were to investigate the modifying effects of 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), a genotoxic carcinogen produced during cooking of protein-rich foods, and elucidate underlying mechanisms in a two-stage hepatocarcinogenesis mice model. Six-week-old B6C3F1 mice were subjected to two-thirds partial hepatectomy at the beginning of the study, followed by an intraperitoneal injection of diethylnitrosamine on day 1. Starting 1 week later, they were fed diets containing IQ at doses of 30, 100, or 300 ppm for 39 weeks. A dose-dependent trend for increase in eosinophilic altered foci as well as eosinophilic hepatocellular adenomas was observed, along with significant elevation in the incidence of hepatocellular carcinomas in the 100- and 300-ppm IQ groups as compared with initiation control group. Furthermore, IQ elevated the protein expression levels of Wnt1, transforming growth factor-β (TGF-β), TGF-β receptors 1 and 2 (TβR1 and TβR2), and phosphorylated c-Jun (p-c-Jun), while suppressing those of E-cadherin and p21(WAF1/Cip1). Moreover, translocation of β-catenin to the nuclei as well as upregulated nuclear expression of c-Myc and cyclin D1, which are downstream targets of β-catenin and p-c-Jun, were detected at 100 and 300 ppm. These findings suggest that IQ exerts dose-dependent promoting effects on mice hepatocarcinogenesis by activating TGF-β and Wnt/β-catenin signaling pathways and inhibiting cell adhesion.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Western
  • Body Weight / drug effects
  • Carcinoma, Hepatocellular / chemically induced*
  • Carcinoma, Hepatocellular / metabolism
  • Carcinoma, Hepatocellular / pathology
  • Cell Adhesion / drug effects
  • Cell Transformation, Neoplastic / chemically induced*
  • Cell Transformation, Neoplastic / metabolism
  • Cell Transformation, Neoplastic / pathology
  • Diethylnitrosamine
  • Dose-Response Relationship, Drug
  • Drinking / drug effects
  • Eating / drug effects
  • Hepatectomy
  • Immunohistochemistry
  • Liver / drug effects*
  • Liver / metabolism
  • Liver / pathology
  • Liver / surgery
  • Liver Neoplasms, Experimental / chemically induced*
  • Liver Neoplasms, Experimental / metabolism
  • Liver Neoplasms, Experimental / pathology
  • Male
  • Mice
  • Organ Size / drug effects
  • Quinolines / toxicity*
  • Time Factors
  • Transforming Growth Factor beta / metabolism*
  • Wnt Proteins / metabolism*
  • Wnt Signaling Pathway / drug effects*
  • beta Catenin / metabolism*

Substances

  • CTNNB1 protein, mouse
  • Quinolines
  • Transforming Growth Factor beta
  • Wnt Proteins
  • beta Catenin
  • 2-amino-3-methylimidazo(4,5-f)quinoline
  • Diethylnitrosamine