PloS one · 2013
Celecoxib-induced cytotoxic effect is potentiated by inhibition of autophagy in human urothelial carcinoma cells.
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Huang Kuo-How, Kuo Kuan-Lin, Ho I-Lin, Chang Hong-Chiang, Chuang Yuan-Ting, Lin Wei-Chou, Lee Ping-Yi, Chang Shih-Chen, Chiang Chih-Kang, Pu Yeong-Shiau, Chou Chien-Tso, Hsu Chen-Hsun, Liu Shing-Hwa
Аннотация
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.
Предметные рубрики MeSH
AdenineAntineoplastic AgentsAutophagyAutophagy-Related Protein 7Carcinoma, Transitional CellCelecoxibCell Line, TumorCyclooxygenase 2 InhibitorsEndoplasmic Reticulum StressGene Expression Regulation, NeoplasticHumansJNK Mitogen-Activated Protein KinasesMAP Kinase Kinase 4MacrolidesPhosphoproteinsPyrazolesRNA, Small InterferingSignal TransductionSirolimusSulfonamidesUbiquitin-Activating EnzymesUrinary Bladder Neoplasms