Background: p53 is a key regulator of the cellular stress response. p53 modulates the transcription of several genes.
Objectives: To examine the influence of p53 on expression of heat shock protein 72 (HSP72).
Methods: 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.
Results: 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.
Conclusions: p53 status may influence the basal level of HSP72.