An unexpected role for keratin 10 end domains in susceptibility to skin cancer

The study investigated the role of keratin 10 (K10) end domains in skin cancer susceptibility using K1014chim mutant mice. Contrary to expectations, these mice showed increased susceptibility to benign tumor development when exposed to a chemical skin carcinogenesis protocol, developing 2-3 times more tumors than wild-type controls. The study found that the presence of K10 end domains did not suppress keratinocyte proliferation but instead reduced apoptosis in response to environmental stressors like UV-B radiation and TNFα. This suggested that K10 end domains might interfere with apoptotic mediators, highlighting a complex role in promoting tumor growth and reducing apoptosis, which could inform future therapeutic strategies.