Silencing of COX-2 by RNAi modulates epithelial-mesenchymal transition in breast cancer cells partially dependent on the PGE2 cascade.

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 PGE2 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.
Authors	Juan Cao, Xiao Yang, Wen-Tong Li, Chun-Ling Zhao, Shi-Jun Lv
Journal	Asian Pacific journal of cancer prevention : APJCP (Asian Pac J Cancer Prev) Vol. 15 Issue 22 Pg. 9967-72 ( 2014) ISSN: 2476-762X [Electronic] Thailand
PMID	25520137 (Publication Type: Journal Article)
Chemical References	Cadherins Cyclooxygenase 2 Inhibitors Pyrazoles RNA, Messenger RNA, Small Interfering Sulfonamides Cyclooxygenase 2 PTGS2 protein, human Proto-Oncogene Proteins c-akt Celecoxib Dinoprostone
Topics	Apoptosis (drug effects) Blotting, Western Breast Neoplasms (drug therapy, metabolism, pathology) Cadherins (genetics, metabolism) Celecoxib Cell Adhesion (drug effects) Cell Movement (drug effects) Cell Proliferation (drug effects) Cyclooxygenase 2 (chemistry, genetics, metabolism) Cyclooxygenase 2 Inhibitors (pharmacology) Dinoprostone (metabolism) Epithelial-Mesenchymal Transition (drug effects, genetics) Female Flow Cytometry Fluorescent Antibody Technique Gene Silencing Humans Immunoenzyme Techniques Proto-Oncogene Proteins c-akt (genetics, metabolism) Pyrazoles (pharmacology) RNA, Messenger (genetics) RNA, Small Interfering (genetics) Real-Time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Sulfonamides (pharmacology) Tumor Cells, Cultured

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