Aflatoxin B1 negatively regulates Wnt/β-catenin signaling pathway through activating miR-33a

PLoS One. 2013 Aug 27;8(8):e73004. doi: 10.1371/journal.pone.0073004. eCollection 2013.

Abstract

MicroRNAs are known to play an important role in modulating gene expression in various diseases including cancers and cardiovascular disorders, but only a few of them are associated with the pathology of aflatoxin B1 (AFB1), a potent mycotoxin. Here, we discovered a novel regulatory network between AFB1, miR-33a and β-catenin in human carcinoma cells. The level of miR-33a was up-regulated in hepatocellular carcinoma (HCC) cells treated with AFB1, while in the same cells causing the decrease in β-catenin expression when treated at their IC50 values. miR-33a, specifically miR-33a-5p, was demonstrated to down-regulate the expression of β-catenin, affect the β-catenin pathway, and inhibit cell growth. Also, by employing a luciferase assay, we found that miR-33a down-regulated β-catenin by directly binding to the 3'-UTR of β-catenin. These results suggested that AFB1 might down-regulate β-catenin by up-regulating miR-33a. This understanding opens new lines of thought in the potential role of miR-33a in the clinical therapy of cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3' Untranslated Regions
  • Aflatoxin B1 / pharmacology*
  • Down-Regulation / drug effects
  • Gene Expression Regulation, Neoplastic / drug effects*
  • HeLa Cells
  • Hep G2 Cells
  • Humans
  • MicroRNAs / metabolism*
  • Neoplasm Proteins / biosynthesis*
  • Neoplasms / drug therapy*
  • Neoplasms / metabolism
  • Neoplasms / pathology
  • Poisons / pharmacology*
  • RNA, Neoplasm / metabolism*
  • Wnt Proteins / metabolism*
  • Wnt Signaling Pathway / drug effects*
  • beta Catenin / biosynthesis*

Substances

  • 3' Untranslated Regions
  • MIRN33a microRNA, human
  • MicroRNAs
  • Neoplasm Proteins
  • Poisons
  • RNA, Neoplasm
  • Wnt Proteins
  • beta Catenin
  • Aflatoxin B1

Grants and funding

This work was supported by the National Natural Science Foundation of China (No. 31000961 and No. 31172297), and the Natural Science Foundation of Fujian Province (No. 2013J01081). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.