FOXA1 Induces E-Cadherin Expression at the Protein Level <i>via</i> Suppression of Slug in Epithelial Breast Cancer Cells

DOI Web Site Web Site PubMed 3 Citations Open Access
  • Anzai Erina
    Laboratory of Molecular Cell Biology, Graduate School of Pharmaceutical Sciences, Chiba University
  • Hirata Kensuke
    Laboratory of Molecular Cell Biology, Graduate School of Pharmaceutical Sciences, Chiba University
  • Shibazaki Misato
    Laboratory of Molecular Cell Biology, Graduate School of Pharmaceutical Sciences, Chiba University
  • Yamada Chiaki
    Laboratory of Molecular Cell Biology, Graduate School of Pharmaceutical Sciences, Chiba University
  • Morii Mariko
    Laboratory of Molecular Cell Biology, Graduate School of Pharmaceutical Sciences, Chiba University
  • Honda Takuya
    Laboratory of Molecular Cell Biology, Graduate School of Pharmaceutical Sciences, Chiba University
  • Yamaguchi Naoto
    Laboratory of Molecular Cell Biology, Graduate School of Pharmaceutical Sciences, Chiba University
  • Yamaguchi Noritaka
    Laboratory of Molecular Cell Biology, Graduate School of Pharmaceutical Sciences, Chiba University

Bibliographic Information

Other Title
  • FOXA1 Induces E-Cadherin Expression at the Protein Level via Suppression of Slug in Epithelial Breast Cancer Cells

Search this article

Abstract

<p>Epithelial-to-mesenchymal transition (EMT) is an important process during embryonic development and tumor progression by which adherent epithelial cells acquire mesenchymal properties. Forkhead box protein A1 (FOXA1) is a transcriptional regulator preferentially expressed in epithelial breast cancer cells, and its expression is lost in mesenchymal breast cancer cells. However, the implication of this biased expression of FOXA1 in breast cancer is not fully understood. In this study, we analyzed the involvement of FOXA1 in EMT progression in breast cancer, and found that stable expression of FOXA1 in the mesenchymal breast cancer MDA-MB-231 cells strongly induced the epithelial marker E-cadherin at the mRNA and protein levels. Furthermore, stable expression of FOXA1 was found to reduce the mRNA and protein expression of Slug, a repressor of E-cadherin expression. FOXA1 knockdown in the epithelial breast cancer MCF7 cells reduced E-cadherin protein expression without decreasing its mRNA expression. In addition, FOXA1 knockdown in MCF7 cells up-regulated Slug mRNA and protein expression. Notably, similar to FOXA1 knockdown, stable expression of Slug in MCF7 cells reduced E-cadherin protein expression without decreasing its mRNA expression. Taken together, these results suggest that although FOXA1 can induce E-cadherin mRNA expression, it preferentially promotes E-cadherin expression at the protein level by suppressing Slug expression in epithelial breast cancer, and that the balance of this FOXA1-Slug axis regulates EMT progression.</p>

Journal

Citations (3)*help

See more

Related Projects

See more

Keywords

Details 詳細情報について

Report a problem

Back to top