Celecoxib-induced cytotoxic effect is potentiated by inhibition of autophagy in human urothelial carcinoma cells

PloS One
Kuo-How HuangShing-Hwa Liu

Abstract

Celecoxib, a cyclooxygenase-2 (COX-2) inhibitor, can elicit anti-tumor effects in various malignancies. Here, we sought to clarify the role of autophagy in celecoxib-induced cytotoxicity in human urothelial carcinoma (UC) cells. The results shows celecoxib induced cellular stress response such as endoplasmic reticulum (ER) stress, phosopho-SAPK/JNK, and phosopho-c-Jun as well as autophagosome formation in UC cells. Inhibition of autophagy by 3-methyladenine (3-MA), bafilomycin A1 or ATG7 knockdown potentiated celecoxib-induced apoptosis. Up-regulation of autophagy by rapamycin or GFP-LC3B-transfection alleviated celecoxib-induced cytotoxicity in UC cells. Taken together, the inhibition of autophagy enhances therapeutic efficacy of celecoxib in UC cells, suggesting a novel therapeutic strategy against UC.

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Citations

Oct 11, 2014·Journal of Cellular Physiology·Laurence BoothPaul Dent
Nov 26, 2016·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Ying LuLing-Ling Liu
Jun 8, 2019·International Journal of Molecular Medicine·Feng LiuJingtao Zhong
Jul 2, 2020·Cancer Management and Research·Xiangjie FuPeijun Liu
Oct 20, 2018·International Journal of Oncology·George Mihai NitulescuDenisa Margina
Dec 21, 2020·Chemical Biology & Drug Design·Bashir AhmadDeog-Hwan Oh
Oct 13, 2021·Expert Opinion on Therapeutic Targets·Pratishtha GuptaMinal Garg

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Methods Mentioned

BETA
xenograft
Flow Cytometry
electrophoresis
transfection
Flowcytometry

Software Mentioned

Image J
GraphPad Prism®

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