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J. Biol. Chem., Vol. 278, Issue 51, 51143-51149, December 19, 2003

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PKC Is a Unique Regulator for hsp90 Gene in Heat Shock Response^*

Jian-Min Wu, Lei Xiao¶, Xiao-Kuan Cheng, Lian-Xian Cui, 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 and Shands Cancer Center and Department of Anatomy and Cell Biology, University of Florida, Gainesville, Florida 32610

An early event in cellular heat shock response is the transmittance of stress signals from the cell surface into the nuclei, resulting in the induction of heat shock proteins (Hsps). Protein kinase C (PKC) has been implicated as a key player in transducing stress signals. However, mechanism(s) by which PKC regulates heat shock-induced events remains largely unknown. Here we present data that pan-PKC inhibitor GF109203X, but not classic PKC inhibitor Gö6976, specifically repressed heat shock-induced accumulation of mRNA as well as promoter activity of hsp90, but not hsp90, in Jurkat cells. Subcellular fractionation studies revealed that heat shock exclusively induced PKC- membrane translocation. Consistently, expression of a constitutively active PKC-(A159E) resulted in an enhanced promoter activity of hsp90 upon heat shock, whereas a dominant-negative PKC-(K437R) abolished this effect. In contrast, constitutively active-PKC- or dominant-negative-PKC- had no effects on heat shock induction of the gene. The effect of PKC- on hsp90 expression seems to be stimuli-specific, as phorbol myristate acetate-mediated hsp90 expression was PKC--independent. We conclude that PKC- is specifically required in the signaling pathway leading to the induction of hsp90 gene in response to heat shock.

Received for publication, May 27, 2003 , and in revised form, October 3, 2003.

^* This work was supported by National Natural Sciences Foundation of China Grant 39930050 (to Y.-F. S.) and in part by National Institutes of Health Grant R01-CA88815 (to L. X.). 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.

^¶ To whom correspondence should be addressed: Univ. of Florida Shands Cancer Center, Box 100232, 1600 SW Archer Rd., Gainesville, FL 32610. Tel.: 352-846-1199; Fax: 352-392-5802; E-mail: lxiao{at}ufl.edu.

^|| To whom correspondence should be addressed: Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, 5 Dongdan Santiao, Beijing 100005, China. Tel.: 86-10-6529-6416; Fax: 86-10-6526-9665; E-mail: yfshen{at}imicams.ac.cn or yfscams{at}yahoo.com.

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