Up-regulated miR155 reverses the epithelial-mesenchymal transition induced by EGF and increases chemo-sensitivity to cisplatin in human Caski cervical cancer cells

PLoS One. 2012;7(12):e52310. doi: 10.1371/journal.pone.0052310. Epub 2012 Dec 20.

Abstract

The epithelial-mesenchymal transition (EMT) induced by EGF promotes cervical cancer progression; however, the mechanisms underlying the EGF-induced EMT remain unclear. In this study, we reported that miR155 overexpression suppressed EGF-induced EMT, decreased migration/invasion capacities, inhibited cell proliferation and increased the chemo-sensitivity to DDP in human Caski cervical cancer cells. Further, the overexpression of miR155 increased TP53 expression but reduced SMAD2, and CCND1 expression levels. These data suggest that miR155 negatively regulates EGF-induced EMT. We conclude that miR155 does not act as an oncogene but as a tumour suppressor in Caski cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blotting, Western
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Movement / physiology
  • Cell Proliferation / drug effects
  • Cisplatin / pharmacology*
  • Epidermal Growth Factor / pharmacology*
  • Epithelial-Mesenchymal Transition / drug effects*
  • Epithelial-Mesenchymal Transition / genetics
  • Female
  • Fluorescent Antibody Technique
  • Humans
  • MicroRNAs / genetics*
  • Uterine Cervical Neoplasms / genetics*

Substances

  • MicroRNAs
  • Epidermal Growth Factor
  • Cisplatin

Grants and funding

Financial support for this work was provided by the Natural Science Foundation of Hubei province (Grant no. 2011CDB181), Independent Research Fund, Wuhan University (no. 201130302020016). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.