Cyclooxygenase-2 promotes ovarian cancer cell migration and cisplatin resistance via regulating epithelial mesenchymal transition.
- Author:
Lin DENG
1
;
Ding-Qing FENG
1
;
Bin LING
1
Author Information
- Publication Type:Journal Article
- Keywords: Ovarian cancer (OC); Cyclooxygenase-2 (COX-2); Drug resistance; Migration; Epithelial-mesenchymal transition (EMT)
- MeSH: Celecoxib/pharmacology*; Cell Line, Tumor; Cell Movement; Cisplatin/pharmacology*; Cyclooxygenase 2/physiology*; Drug Resistance, Neoplasm; Epithelial-Mesenchymal Transition; Female; Humans; Ovarian Neoplasms/pathology*; Polymerase Chain Reaction
- From: Journal of Zhejiang University. Science. B 2020;21(4):315-326
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:Drug-resistance and metastasis are major reasons for the high mortality of ovarian cancer (OC) patients. Cyclooxygenase-2 (COX-2) plays a critical role in OC development. This study was designed to evaluate the effects of COX-2 on migration and cisplatin (cis-dichloro diammine platinum, CDDP) resistance of OC cells and explore its related mechanisms.
METHODS:Cell counting kit-8 (CCK-8) assay was used to detect the cytotoxicity effects of celecoxib (CXB) and CDDP on SKOV3 and ES2 cells. The effect of COX-2 on migration was evaluated via the healing test. Western blot and real-time quantitative polymerase chain reaction (qPCR) were used to analyze E-cadherin, vimentin, Snail, and Slug levels.
RESULTS:COX-2 promoted drug-resistance and cell migration. CXB inhibited these effects. The combination of CDDP and CXB increased tumor cell sensitivity, reduced the amount of CDDP required, and shortened treatment administration time. COX-2 upregulation increased the expression of Snail and Slug, resulting in E-cadherin expression downregulation and vimentin upregulation.
CONCLUSIONS:COX-2 promotes cancer cell migration and CDDP resistance and may serve as a potential target for curing OC.
