Heat stress: A risk factor for skin carcinogenesis [journal article]
Document Type
Journal Article
Keywords
[RSTDPub], Heat shock proteins, Heat shock response, Heat stress, HSP72, HSP90, Skin cancerchaperone, heat shock protein, heat shock protein 72, heat shock protein 90, mitogen activated protein kinase, mutant protein, protein p53, stress activated protein kinase, apoptosis, cancer risk, cell function, cell proliferation, cell survival, gene mutation, heat stress, human, nonhuman, oncogene, priority journal, protein expression, protein function, risk factor, short survey, signal transduction, skin carcinogenesis, thermal exposure, ultraviolet radiation, Heat shock proteins, Heat shock response, Heat stress, HSP72, HSP90, Skin cancer, Animals, Heat-Shock Proteins, Hot Temperature, Humans, JNK Mitogen-Activated Protein Kinases, Risk Factors, Signal Transduction, Skin Neoplasms, Tumor Suppressor Protein p53, Ultraviolet Rays
Publisher
Elsevier Ireland Ltd
Faculty
Faculty of Health, Engineering and Science
School
School of Medical Sciences
RAS ID
16388
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.
Comments
Calapre, L. D., Gray, E. S., & Ziman, M. R. (2013). Heat stress: a risk factor for skin carcinogenesis. Cancer Letters, 337(1), 35-40. Available here