Imiquimod activates p53-dependent apoptosis in a human basal cell carcinoma cell line

Highlights • IMQ induces p53 expression and activation in skin cancer cells in a TLR7/8-independent manner. • The IMQ-induced p53 expression and activation are achieved through increased ROS production to stimulate the ATM/ATR-Chk1/Chk2 axis. • Genetic silencing of p53 significantly decreases the IM...

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Veröffentlicht in:	Journal of dermatological science 2016-03, Vol.81 (3), p.182-191
Hauptverfasser:	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
Format:	Artikel
Sprache:	eng
Schlagworte:	Active Transport, Cell Nucleus Aminoquinolines - pharmacology Antineoplastic Agents - pharmacology Apoptosis Apoptosis - drug effects Ataxia Telangiectasia Mutated Proteins - genetics Ataxia Telangiectasia Mutated Proteins - metabolism Autophagy Autophagy - drug effects Carcinoma, Basal Cell - drug therapy Carcinoma, Basal Cell - genetics Carcinoma, Basal Cell - metabolism Carcinoma, Basal Cell - pathology Cell Line, Tumor Dermatology Dose-Response Relationship, Drug Gene Expression Regulation, Neoplastic Humans Imiquimod Mutation p53 Phosphorylation Reactive Oxygen Species - metabolism RNA Interference Signal Transduction - drug effects Skin Neoplasms - drug therapy Skin Neoplasms - genetics Skin Neoplasms - metabolism Skin Neoplasms - pathology Time Factors Transfection Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism
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Zusammenfassung:	Highlights • IMQ induces p53 expression and activation in skin cancer cells in a TLR7/8-independent manner. • The IMQ-induced p53 expression and activation are achieved through increased ROS production to stimulate the ATM/ATR-Chk1/Chk2 axis. • Genetic silencing of p53 significantly decreases the IMQ-induced caspase cascade activation and apoptosis but enhances autophagy. • p53 mutant cell lines are more resistant to IMQ-induced apoptosis than p53 wildtype cell lines.
ISSN:	0923-1811 1873-569X
DOI:	10.1016/j.jdermsci.2015.12.011