Abstract
Abstract Caveolin-1 (Cav1) is the main protein component of a specialized form of lipid raft termed caveolae and serves to compartmentalize and negatively regulate the activity of signaling molecules involved in cell proliferation and survival. Cav1 has been shown to act as a tumor suppressor in several types of cancer, including breast cancer and melanoma, but its role in the pathogenesis of non-melanoma skin cancer remains largely unexplored. Previous work has indicated that Cav1 is expressed in the basal cell layer of both murine and human epidermis; additionally, loss of Cav1 protein has been shown by our lab to render murine skin more susceptible to papilloma development following treatment with a carcinogenic compound. The purpose of the current study was to further examine the role of Cav1 in non-melanoma skin cancer development using various experimental approaches. Given the previous research, our hypothesis is that Cav1 acts as a suppressor of tumor growth and development in the skin. In order to explore this hypothesis, we have used several experimental systems, including human tissue arrays and loss of function and gain of function studies in animal models of cutaneous squamous cell carcinoma. Manipulation of Cav1 expression in (1) a keratinocyte cell line followed by xenotransplantation and (2) an induced model of skin cancer allowed us to assess the effect of this protein on tumor development, growth, and progression. Using these approaches, we were able to show that Cav1 ablation dramatically increases not only in vitro cell growth and invasion, but also in vivo tumorigenesis, tumor growth, and invasion. In conclusion, these studies provide further evidence in support of the hypothesis that Cav1 acts as a tumor suppressor protein in the skin and serve to identify new potential therapeutic targets in the treatment of cutaneous malignancies. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1083. doi:10.1158/1538-7445.AM2011-1083
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