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標題: Imiquimod activates p53-dependent apoptosis in a human basal cell carcinoma cell line
作者: Huang, Shi-Wei
Chang, Shu-Hao
Mu, Szu-Wei
Jiang, Hsin-Yi
Wang, Sin-Ting
Kao, Jun-Kai
Huang, Jau-Ling
Wu, Chun-Ying
Chen, Yi-Ju
Shieh, Jeng-Jer
關鍵字: Apoptosis;Autophagy;Imiquimod;p53;Active Transport, Cell Nucleus;Aminoquinolines;Antineoplastic Agents;Apoptosis;Ataxia Telangiectasia Mutated Proteins;Autophagy;Carcinoma, Basal Cell;Cell Line, Tumor;Dose-Response Relationship, Drug;Gene Expression Regulation, Neoplastic;Humans;Mutation;Phosphorylation;RNA Interference;Reactive Oxygen Species;Signal Transduction;Skin Neoplasms;Time Factors;Transfection;Tumor Suppressor Protein p53
Project: Journal of dermatological science, Volume 81, Issue 3, Page(s) 182-91.
The tumor suppressor p53 controls DNA repair, cell cycle, apoptosis, autophagy and numerous other cellular processes. Imiquimod (IMQ), a synthetic toll-like receptor (TLR) 7 ligand for the treatment of superficial basal cell carcinoma (BCC), eliminates cancer cells by activating cell-mediated immunity and directly inducing apoptosis and autophagy in cancer cells.
DOI: 10.1016/j.jdermsci.2015.12.011
Appears in Collections:生物醫學研究所

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