Kindlin 2 promotes breast cancer invasion via epigenetic silencing of the microRNA200 gene family

Int J Cancer. 2013 Sep 15;133(6):1368-79. doi: 10.1002/ijc.28151. Epub 2013 Apr 11.

Abstract

Kindlin 2, as a focal adhesion protein, controls integrin activation and regulates Wnt signaling in an integrin-binding independent manner. However, the association of Kindlin 2 with cancer-related microRNAs is unknown. Here, we report that Kindlin 2 markedly downregulates the expression of miR-200 family by inducing CpG island hypermethylation. Mechanistically, Kindlin 2 forms a complex with DNMT3A in the cell nucleus and the two proteins co-occupy the promoter of miRNA-200b. Functionally, repression of miR-200b is required for Kindlin 2-induced breast cancer cell invasion and tumor formation. Our data indicate that Kindlin 2 plays a novel role in epigenetic repression of miR-200 family, a mechanism that promotes breast cancer invasion.

Keywords: DNA methyltransferase; Kindlins; MicroRNA-200 family; breast cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Breast Neoplasms / pathology*
  • Cell Line, Tumor
  • CpG Islands
  • DNA (Cytosine-5-)-Methyltransferases / physiology
  • DNA Methylation
  • DNA Methyltransferase 3A
  • Female
  • Gene Silencing*
  • Humans
  • Membrane Proteins / physiology*
  • Mice
  • Mice, SCID
  • MicroRNAs / genetics*
  • Neoplasm Invasiveness
  • Neoplasm Proteins / physiology*

Substances

  • DNMT3A protein, human
  • Dnmt3a protein, mouse
  • FERMT3 protein, human
  • MIRN200 microRNA, human
  • Membrane Proteins
  • MicroRNAs
  • Neoplasm Proteins
  • DNA (Cytosine-5-)-Methyltransferases
  • DNA Methyltransferase 3A