p53-dependent regulation of heat shock protein 72.
BACKGROUND
p53 is a key regulator of the cellular stress response. p53 modulates the transcription of several genes.


OBJECTIVE
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.
Quenneville
L A
LA
Department of Pathology, University of British Columbia, Vancouver, British Columbia, Canada.
Trotter
M J
MJ
Maeda
T
T
Tron
V A
VA
D000818:Animals; D015153:Blotting, Western; D002294:Carcinoma, Squamous Cell / Q000378:metabolism; D018929:Cell Culture Techniques; D016158:Genes, p53 / Q000502:physiology*; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000378:metabolism*; D015603:Keratinocytes / Q000378:metabolism*; D008545:Melanoma / Q000378:metabolism; D051379:Mice; D009363:Neoplasm Proteins / Q000378:metabolism; D027383:Papillomaviridae; D030361:Papillomavirus Infections / Q000378:metabolism; D012878:Skin Neoplasms / Q000378:metabolism; D014412:Tumor Virus Infections / Q000378:metabolism
D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D009363:Neoplasm Proteins