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Volume 272, Number 43, Issue of October 24, 1997 pp. 26803-26806
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

COMMUNICATION:
Heat Shock Factor 1 Represses Ras-induced Transcriptional Activation of the c-fos Gene

(Received for publication, May 22, 1997, and in revised form, July 17, 1997)

Changmin Chen , Yue Xie , Mary Ann Stevenson , Philip E. Auron ^§ and Stuart K. Calderwood

From the  Dana-Farber Cancer Institute and Joint Center for Radiation Therapy, Harvard Medical School, Boston, Massachusetts 02115 and the ^§ Center for Blood Research, Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115

Heat shock factor 1, the critical molecular regulator of the stress response is conserved throughout eukaryotic organisms and activates the transcription of heat shock genes. We now show that heat shock factor 1 inhibits the expression of c-fos, an immediate early gene that controls responses to extracellular stimuli for growth and differentiation. Heat shock factor 1 inhibits the transcription of the c-fos gene and antagonizes the activating effects of the signal transducing protein Ras on the c-fos promoter and on the promoter of another Ras responsive gene uPA. This property was specific for heat shock factor 1; c-fos repression was not seen with the structurally related protein heat shock factor 2. Repression involved different molecular mechanisms compared with those involved in transcriptional activation by heat shock factor 1 and specifically did not require binding to the c-fos promoter. Thus, in addition to its known role as a transcriptional activator of the cellular heat shock response, heat shock factor 1 also antagonizes the expression of Fos, a key component of the ubiquitous AP-1 transcription factor complex and as such could influence multiple aspects of cell regulation.

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