Stable transfection of estrogen receptor-alpha suppresses expression of cyclooxygenase-2 and vascular endothelial growth factor-C in MDA-MB-231 breast cancer cells

Chin Med J (Engl). 2010 Aug 5;123(15):1989-94.

Abstract

Background: Estrogen receptor (ER)-negative breast cancer cells are more aggressive than ER-positive cells. Elevated levels of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor-C (VEGF-C) expression have been detected in cultured human breast cancer cells and are associated with negative hormone receptor status. In this study, we created ERalpha stable transfectants in MDA-MB-231 cells to explore the effect of ERalpha on cell growth and COX-2 and VEGF-C expression.

Methods: The green fluorescent protein (GFP)-ERalpha plasmids were stably transfected into ER-negative MDA-MB-231 cells. The proliferation and migration of untransfected MDA-MB-231 cells, ERalpha-transfected MDA-MB-231 cells and ER-positive MCF-7 cells were determined. The expression of COX-2, and the levels of VEGF-C mRNA and the VEGF-C secretion concentration were assayed in these cell lines.

Results: The proliferation and migration capacities of ERalpha-tranfected MDA-MB-231 cells were significantly decreased (P < 0.05). The expression of COX-2 was significantly lower in ERalpha-tranfected MDA-MB-231 cells than in untranfected MDA-MB-231 cells. The mRNA and protein levels of VEGF-C were lower in ERalpha-tranfected MDA-MB-231 cells than in untransfected MDA-MB-231 cells (P < 0.05).

Conclusions: ERalpha stable transfection inhibits proliferation and migration capacities of MDA-MB-231 cells and decreases expression of COX-2 and VEGF-C. The decreases of proliferation and migration capacities may be related to suppression of COX-2 and VEGF-C expression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blotting, Western
  • Breast Neoplasms / genetics
  • Breast Neoplasms / metabolism*
  • Cell Cycle / genetics
  • Cell Cycle / physiology
  • Cell Line, Tumor
  • Cell Movement / genetics
  • Cell Movement / physiology
  • Cell Proliferation
  • Cyclooxygenase 2 / genetics
  • Cyclooxygenase 2 / metabolism*
  • Enzyme-Linked Immunosorbent Assay
  • Estrogen Receptor alpha / genetics
  • Estrogen Receptor alpha / metabolism*
  • Female
  • Flow Cytometry
  • Humans
  • Polymerase Chain Reaction
  • Transfection
  • Vascular Endothelial Growth Factor C / genetics
  • Vascular Endothelial Growth Factor C / metabolism*

Substances

  • Estrogen Receptor alpha
  • Vascular Endothelial Growth Factor C
  • Cyclooxygenase 2
  • PTGS2 protein, human