p53-dependent regulation of heat shock protein 72

• Published in: British journal of dermatology (1951) Vol. 146; no. 5; pp. 786 - 791
• Main Authors: Quenneville, L.A., Trotter, M.J., Maeda, T., Tron, V.A.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.05.2002; Blackwell; Oxford University Press
• Subjects: Animals; Biological and medical sciences; Blotting, Western; Carcinoma, Squamous Cell - metabolism; Cell Culture Techniques; Dermatology; Genes, p53 - physiology; heat shock protein 72; Heat-Shock Proteins - metabolism; HSP72 Heat-Shock Proteins; human papillomavirus; Investigative techniques, diagnostic techniques (general aspects); Keratinocytes - metabolism; Medical sciences; Melanoma - metabolism; Mice; Neoplasm Proteins - metabolism; p53; Papillomaviridae; Papillomavirus Infections - metabolism; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques; Skin Neoplasms - metabolism; squamous cell carcinoma; Tumor Virus Infections - metabolism; Human; Cell culture; Squamous cell carcinoma; Rodentia; Papovaviridae; Human papillomavirus 18; Papillomavirus; Virus; Human papillomavirus 16; Human papillomavirus; Vertebrata; Regulation(control); Mammalia; TP53 Gene; Mouse; Animal; Heat shock protein; Keratinocyte; Skin; Tumor suppressor gene
• ISSN: 0007-0963; 1365-2133
• DOI: 10.1046/j.1365-2133.2002.04721.x

Summary 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.