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UV-irradiation is the major cause of skin squamous cell cancer (SCC) that results from uncontrolled growth of abnormal squamous cells. The exposure of skin cells to UV-irradiation causes DNA damage that leads to outgrowth of abnormal skin cells with decreased apoptosis, tumorigenesis and cancers. This study is to determine the roles of Krüppel-like factor 4 (KLF4) related to the repair pathway in UV-induced skin damage and SCC. KLF4 is involved in various epithelial cancers including SCC.  However, the roles of KLF4 in UV-mediated SCC have not yet been defined. We hypothesize that the loss of KLF4 in-vivo followed by UV irradiation leads to increased cell proliferation and decreased apoptosis of skin cells that facilitate UV-mediated SCC. To determine the roles of KLF4 in UV-irradiation induced SCC, we will evaluate the effects of KLF4 loss on 1) skin cell proliferation by immunohistochemistry (IHC) for BrdU and 2) apoptosis by TUNEL staining. This fall semester, I will conduct about 60-IHC stainings for BrdU and TUNEL, and perform 300-microscopy image analyses. We expect that absence of KLF4 will lead to increased proliferation and decreased apoptosis. These changes will lead to early appearance of tumor. Thus, these proposed studies would provide new insights on cellular responses underlying roles of KLF4 in UV-mediated SCC. Furthermore, the experience of working on this project and their potential to improve the lives of so many patients will be incredibly rewarding in shedding light on what I hope to do with my life, and will firmly established my intellectual interests in biological sciences.

UV-irradiation is the major cause of skin squamous cell cancer (SCC) that results from uncontrolled growth of abnormal squamous cells. The exposure of skin cells to UV-irradiation causes DNA damage that leads to outgrowth of abnormal skin cells with decreased apoptosis, tumorigenesis and cancers. This study is to determine the roles of Krüppel-like factor 4 (KLF4) related to the repair pathway in UV-induced skin damage and SCC. KLF4 is involved in various epithelial cancers including SCC.  However, the roles of KLF4 in UV-mediated SCC have not yet been defined. We hypothesize that the loss of KLF4 in-vivo followed by UV irradiation leads to increased cell proliferation and decreased apoptosis of skin cells that facilitate UV-mediated SCC. To determine the roles of KLF4 in UV-irradiation induced SCC, we will evaluate the effects of KLF4 loss on 1) skin cell proliferation by immunohistochemistry (IHC) for BrdU and 2) apoptosis by TUNEL staining. This fall semester, I will conduct about 60-IHC stainings for BrdU and TUNEL, and perform 300-microscopy image analyses. We expect that absence of KLF4 will lead to increased proliferation and decreased apoptosis. These changes will lead to early appearance of tumor. Thus, these proposed studies would provide new insights on cellular responses underlying roles of KLF4 in UV-mediated SCC. Furthermore, the experience of working on this project and their potential to improve the lives of so many patients will be incredibly rewarding in shedding light on what I hope to do with my life, and will firmly established my intellectual interests in biological sciences.