School of Medical Science, Edith Cowan University, Perth, Western Australia, Australia.
Cancer Lett. 2013 Aug 28;337(1):35-40. doi: 10.1016/j.canlet.2013.05.039. Epub 2013 Jun 5.
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.
最近的证据表明，热应激也可能是皮肤致癌的一个风险因素。热应激会导致热休克蛋白（HSPs）的激活，HSPs 是一种伴侣蛋白，可以防止细胞凋亡，确保其细胞功能。然而，HSPs 的募集也可能产生有害影响，特别是如果从凋亡中拯救出来的细胞带有致癌突变。我们假设，热和 UV 的同时暴露会通过 HSPs 和致癌突变蛋白的同时表达来诱导皮肤癌。在这里，我们回顾了一些研究，这些研究表明，热应激激活的热休克蛋白，如 HSP72 和 HSP90，可以影响 MAPK、JNK 和 p53 等信号通路，这些通路都参与调节细胞增殖、存活和凋亡。
