FoxD3 deficiency promotes breast cancer progression by induction of epithelial-mesenchymal transition

Biochem Biophys Res Commun. 2014 Apr 4;446(2):580-4. doi: 10.1016/j.bbrc.2014.03.019. Epub 2014 Mar 12.

Abstract

The transcription factor forkhead box D3 (FOXD3) plays an important role in the development of neural crest and gastric cancer cells. However, the function and mechanisms of FOXD3 in the breast tumorigenesis and progression is still limited. Here, we report that FOXD3 is a tumor suppressor of breast cancer tumorigenicity and aggressiveness. We found that FOXD3 is down-regulated in breast cancer tissues. Patients with low FOXD3 expression have a poor outcome. Depletion of FOXD3 expression promotes breast cancer cell proliferation and invasion in vitro, whereas overexpression of FOXD3 inhibits breast cancer cell proliferation and invasion both in vitro and in vivo. In addition, depletion of FOXD3 is linked to epithelial-mesenchymal transition (EMT)-like phenotype. Our results indicate FOXD3 exhibits tumor suppressive activity and may be useful for breast therapy.

Keywords: Breast cancer; Epithelial–mesenchymal transition; FoxD3.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology*
  • Cell Line, Tumor
  • Cell Proliferation
  • Epithelial-Mesenchymal Transition*
  • Female
  • Forkhead Transcription Factors / deficiency*
  • Forkhead Transcription Factors / genetics
  • Forkhead Transcription Factors / metabolism*
  • Humans
  • Neoplasm Invasiveness

Substances

  • FOXD3 protein, human
  • Forkhead Transcription Factors