HSP105 suppresses the progression of cutaneous squamous cell carcinoma by activating the P53 signaling pathway.

Cutaneous squamous cell carcinoma (cSCC) is a common type of nonmelanoma skin cancer with a very high incidence. Heat shock proteins (HSPs) are involved in abnormal proliferation, invasion and apoptosis of tumor cells. Whether HSP105 acts as a promoter or inhibitor of cSCC remains to be further explored. This study investigated the biological role of HSP105 in the progression of cSCC. Real-time PCR and Western blotting were used to detect the mRNA and protein expression of HSP105 in cSCC cell lines. Cell lines with overexpression and knockdown of HSP105 were established to analyze their cell cycle distribution, proliferation, apoptosis, migration, invasion and biological mechanisms. Finally, the proliferative effect of HSP105 in cSCC cells was verified in nude mice. We found that HSP105 expression was decreased in cSCC cell lines. Overexpression of HSP105 in A431 and SCL-1 cell lines induced cell cycle arrest and apoptosis, inhibited cell proliferation, reduced cell migration and invasion, and inhibited tumor growth in vivo. The opposite result was observed in the HSP105-silenced cell lines. Furthermore, HSP105 activated the P53 signaling pathway and exerted anticancer effects. Our findings provide new perspectives on the critical role and potential mechanisms of HSP105 in the development of cSCC, suggesting that HSP105 may be a novel therapeutic target for cSCC.