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J. Biol. Chem., Vol. 279, Issue 41, 42545-42551, October 8, 2004

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Repression of hsp90 Gene by p53 in UV Irradiation-induced Apoptosis of Jurkat Cells^*

Ye Zhang, Jin-Shan Wang, Li-Ling Chen, Yong Zhang, Xiao-Kuan Cheng, Feng-Yan Heng, Ning-Hua Wu, and Yu-Fei Shen

From the National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100005, China

Tumor suppressor p53 has been implicated in cell stress response and determines cell fate of either growth arrest or apoptosis. Heat shock proteins (Hsps) expressed under stress usually confer survival protection to the cell or interruption in the apoptotic pathways. Although Hsp90 can physically interact with p53, whether or not the hsp90 gene is influenced downstream of p53 in UV irradiation-induced apoptosis remains unclear. We have found that the level of p53 is elevated with the decline of Hsp90 in UV-irradiated cells and that malfunction of Hsp90, as inhibited by geldanamycin, enhances the p53-involved UV irradiation-induced apoptosis. In addition, the expression of the hsp90 gene was reduced in both UV-irradiated and wild type p53-transfected cells. These results suggest a negative correlation between the trans factor p53 and a chaperone gene hsp90 in apoptotic cells. Mutation analysis demonstrated that the p53 binding site in the first exon was indispensable for p53 regulation on the hsp90 gene. In addition, with p53 bound at the promoter of the hsp90 gene, mSin3a and p300 were differentially recruited in UV irradiation-treated or untreated Jurkat cells in vivo. The evidence of p53-repressed hsp90 gene expression in UV-irradiated cells shed light on a novel pathway of Hsp90 in the survival control of the stressed cells.

Received for publication, December 28, 2003 , and in revised form, July 19, 2004.

^* This work was supported by National Natural Sciences Foundation of China Grant 39930050 (to Y.-F. S.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

These authors contributed equally to this work.

To whom correspondence should be addressed: 5 Dongdan Santiao, Beijing 100005, China. Tel.: 86-10-65296416; Fax: 86-10-65269665; E-mail: yfshen{at}ms.imicams.ac.cn or yfshen{at}pumc.edu.cn.

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