Gambogic acid-induced degradation of mutant p53 is mediated by proteasome and related to CHIP

As an oncoprotein, mutant p53 is a potential tumor‐specific target for cancer therapy. Most mutated forms of the protein are largely accumulated in cancer cells due to their increased stability. In the present study, we demonstrate that mutant p53 protein stability is regulated by gambogic acid (GA)...

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Veröffentlicht in:	Journal of cellular biochemistry 2011-02, Vol.112 (2), p.509-519
Hauptverfasser:	Wang, Jia, Zhao, Qing, Qi, Qi, Gu, Hong-yan, Rong, Jing-jing, Mu, Rong, Zou, Mei-juan, Tao, Lei, You, Qi-dong, Guo, Qing-long
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Blotting, Western Cell Line, Tumor Cell Survival - drug effects Cell Survival - genetics chaperone chip Cycloheximide - pharmacology gambogic acid Humans Immunohistochemistry Immunoprecipitation Mice Mice, Nude mutant P53 Neoplasms - drug therapy Neoplasms - metabolism proteasome Proteasome Endopeptidase Complex - metabolism Protein Binding - drug effects Protein Synthesis Inhibitors - pharmacology Reverse Transcriptase Polymerase Chain Reaction Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Ubiquitin-Protein Ligases - genetics Ubiquitin-Protein Ligases - metabolism Xanthones - pharmacology Xanthones - therapeutic use Xenograft Model Antitumor Assays
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