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Silencing of COX-2 by RNAi Modulates Epithelial-Mesenchymal Transition in Breast Cancer Cells Partially Dependent on the PGE2 Cascade

  • Cao, Juan (Department of Health Care, Weifang Medical University) ;
  • Yang, Xiao (Nursing School, Weifang Medical University) ;
  • Li, Wen-Tong (Department of Pathology, Weifang Medical University) ;
  • Zhao, Chun-Ling (Department of Biology, Weifang Medical University) ;
  • Lv, Shi-Jun (Department of Pathology, Weifang Medical University)
  • Published : 2014.12.18

Abstract

In order to prove whether downregulation of COX-2 (Cyclooxygenase-2) could modulate the epithelial-mesenchymal transition (EMT) of breast cancer, celecoxib and siRNA were respectively used to inhibit COX-2 function and expression in MDA-MB-231 cells. The EMT reversal effect in the RNAi treated group was better than that of the celecoxib group while there were no obvious differences in the medium $PGE_2$ levels between the two groups. The results show that COX-2 pathways may contribute considerably to EMT of breast cancer cells, partially dependent on the PGE2 cascade. Akt2, ZEB2 and Snail were measured to clarify the underlying mechanisms of COX-2 on EMT; COX-2 may modulate EMT of breast cancer by regulating these factors. This finding may be helpful to elucidate the mechanisms of selective COX-2 inhibitor action in EMT modulation in breast cancer.

Keywords

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