ChloroquineV1, Main, Exploration, bibRecord, 001559

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

Identifieur interne : 001559 ( Main/Exploration ); précédent : 001558; suivant : 001560

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

Auteurs : Jia Wang [République populaire de Chine] ; Qing Zhao [République populaire de Chine] ; Qi Qi [République populaire de Chine] ; Hong-Yan Gu [République populaire de Chine] ; Jing-Jing Rong [République populaire de Chine] ; Rong Mu [République populaire de Chine] ; Mei-Juan Zou [République populaire de Chine] ; Lei Tao [République populaire de Chine] ; Qi-Dong You [République populaire de Chine] ; Qing-Long Guo [République populaire de Chine]

Source :

Journal of Cellular Biochemistry [ 0730-2312 ] ; 2011-02.

RBID : ISTEX:04038BD849A5A4DA2348D56F38E83D6ED279BD4C

Abstract

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). Following GA exposure, protein levels of mutant p53 decreased while the mRNA levels were not affected in MDA‐MB‐435 cells, which indicate that GA down‐regulates mutant p53 at post‐transcription level. Co‐treatment with GA and cycloheximide, a protein synthesis inhibitor, induced a decrease of half‐life of mutant p53 protein. These findings indicated that the reduction of mutant p53 by GA was due to the destabilization and degradation of the protein. Furthermore, inhibition of proteasome activity by MG132 blocked GA‐induced down‐regulation of mutant p53, causing mutant p53 accumulation in detergent‐insoluble cellular fractions. Further studies revealed that mutant p53 was ubiquitinated and it was chaperones related ubiquitin ligase carboxy terminus of Hsp70‐interacting protein (CHIP) rather than MDM2 involved in the degradation of mutant p53. In addition, GA prevented Hsp90/mutant p53 complex formation and enhanced interaction of mutant p53 with Hsp70. Depletion of CHIP stabilized mutant p53 in GA treated cells. In conclusion, mutant p53 may be down‐regulated by GA through chaperones‐assisted ubiquitin/proteasome degradation pathway in cancer cells. J. Cell. Biochem. 112: 509–519, 2011. © 2010 Wiley‐Liss, Inc.

Url:

https://api.istex.fr/ark:/67375/WNG-QTVV1X08-5/fulltext.pdf

DOI: 10.1002/jcb.22941

Affiliations:

République populaire de Chine

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Le document en format XML

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<front><div type="abstract" xml:lang="en">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). Following GA exposure, protein levels of mutant p53 decreased while the mRNA levels were not affected in MDA‐MB‐435 cells, which indicate that GA down‐regulates mutant p53 at post‐transcription level. Co‐treatment with GA and cycloheximide, a protein synthesis inhibitor, induced a decrease of half‐life of mutant p53 protein. These findings indicated that the reduction of mutant p53 by GA was due to the destabilization and degradation of the protein. Furthermore, inhibition of proteasome activity by MG132 blocked GA‐induced down‐regulation of mutant p53, causing mutant p53 accumulation in detergent‐insoluble cellular fractions. Further studies revealed that mutant p53 was ubiquitinated and it was chaperones related ubiquitin ligase carboxy terminus of Hsp70‐interacting protein (CHIP) rather than MDM2 involved in the degradation of mutant p53. In addition, GA prevented Hsp90/mutant p53 complex formation and enhanced interaction of mutant p53 with Hsp70. Depletion of CHIP stabilized mutant p53 in GA treated cells. In conclusion, mutant p53 may be down‐regulated by GA through chaperones‐assisted ubiquitin/proteasome degradation pathway in cancer cells. J. Cell. Biochem. 112: 509–519, 2011. © 2010 Wiley‐Liss, Inc.</div>
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Gambogic acid‐induced degradation of mutant p53 is mediated by proteasome and related to CHIP

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

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Abstract

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