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Exquisite sensitivity of the prostate to androgenic steroids has provided support for the development of systemic therapy for prostate cancer for more than seventy years. Standing strategic approach that focused on inhibiting this unique signaling pathwayled to the use of androgen-deprivation and antiandrogen therapyfor LIMKO inhibitor, kinase that acts downstream of the rock topromote actin assembly, blocked the thickening of the skin and reduces b-catenin levels in K14-rock : ER mice. Likewise, the increase in collagen was found to be reduced. To check whether the rocks (Rho-associated coiled-coil forming protein serine /threonine kinase) activation would affect tumor growth andprogression of skin papillomas are caused by chemical twosteptumorigenesis using dimethyl benzal anthracene (DMBA) and 12-Otetradecanoylphorbol-13-acetate (TPA). Through a mechanism that involves mutations HraĊĦe and subsequent MAPkinase activation, skin papillomas appear and a small percentage progress to invasive cancer. When inducible ROCK: ER mice in two-stage chemical carcinogenesis protocol, the induction of ROCK activity increased total papilloma burden andrapid progression of cancer compared with controls. In addition, total and nuclear b-catenin levels were significantly increased inpapillomas of the rock: ER mice, which means that the pathways that regulate the thickening of the skin are also important in tumorprogression. Interestingly, the authors showed that whiletreatment of mouse skin with DMBA / TPA and the ROCKinhibitor Y-27632 resulted in a significantly lower burden of HPVand a lower conversion rate. It will be of great interest to determine the impact of blocking ROCK activity in establishedpapillomas and carcinomas. Evidence that ROCK signaling is often upregulated in human skin cancer. Further work will be required to provide a detailed picture of the level of ROCK andROCK signaling in tumor grade and extend these studies to othertypes of tumors.

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