p53-dependent regulation of heat shock protein 72.

Abstract

p53 is a key regulator of the cellular stress response. p53 modulates the transcription of several genes. To examine the influence of p53 on expression of heat shock protein 72 (HSP72). Two model systems were used. (i) HSP72 expression was studied by Western blot on extracts from p53-proficient or p53-deficient primary mouse keratinocytes, and (ii) archival human anogenital skin from fibroepithelial polyps, human papillomavirus (HPV) 16/18-associated lesions or squamous cell carcinomas (SCCs) was subjected to immunostaining for HSP72. Basal HSP72 expression was higher in keratinocytes from p53-deficient than from p53-proficient mice. Immunostaining for HSP72 was higher in HPV 16/18 lesions and SCCs, which have reduced p53 protein. p53 status may influence the basal level of HSP72.