title: Heat stress: a risk factor for skin carcinogenesis.
abstract: Recent evidence suggests that heat stress may also be a risk factor of skin carcinogenesis. Heat stress causes activation of heat shock proteins (HSPs), chaperone proteins which prevent cells from undergoing apoptosis and ensuring their cellular function. However, HSPs recruitment may also have deleterious effects particularly if the cells rescued from apoptosis carry oncogenic mutations. We hypothesise that exposures to both heat and UV induce skin cancer(s) by concomitant expression of HSPs and oncogenic mutant proteins. Here we review studies demonstrating that heat stress-activated heat shock proteins such as HSP72 and HSP90 can influence signalling pathways such as MAPK, JNK and p53, which are all involved in regulating cell proliferation, survival and apoptosis.
authors.affiliation: School of Medical Science, Edith Cowan University, Perth, Western Australia, Australia.
authors.forename: Leslie
authors.initials: L
authors.lastname: Calapre
authors.forename: Elin S
authors.initials: ES
authors.lastname: Gray
authors.forename: Mel
authors.initials: M
authors.lastname: Ziman
mesh_terms: D000818:Animals; D006360:Heat-Shock Proteins / Q000502:physiology*; D006358:Hot Temperature; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000502:physiology; D012307:Risk Factors; D015398:Signal Transduction; D012878:Skin Neoplasms / Q000209:etiology*; D016159:Tumor Suppressor Protein p53 / Q000502:physiology; D014466:Ultraviolet Rays
chemical_list: D006360:Heat-Shock Proteins; D016159:Tumor Suppressor Protein p53; D048031:JNK Mitogen-Activated Protein Kinases
keywords: HSP72; HSP90; Heat shock proteins; Heat shock response; Heat stress; Skin cancer