【摘 要】
：
It has long been known that excessive mitotic activity due to H-Ras can block keratinocyte differentiation and cause skin cancer.It is not clear whether there are any innate surveillants that are able
【机 构】
：
Cancer and Inflammation Program National Cancer Institute, National Institutes of Health USA
【出 处】
：
BIT‘s2nd Annual World Cancer Congess-2009 (2009第二届癌症大会)
论文部分内容阅读
It has long been known that excessive mitotic activity due to H-Ras can block keratinocyte differentiation and cause skin cancer.It is not clear whether there are any innate surveillants that are able to ensure that keratinocytes undergo terminal differentiation, preventing the disease.IKKα induces keratinocyte terminal differentiation and its reduction promotes skin tumor development.However, its intrinsic function in skin cancer is unknown.Here we found that mice with IKKα deletion in keratinocytes developed a thickened epidermis and spontaneous squamous cell-like carcinomas.Inactivation of epidermal growth factor receptor (EGFR) or reintroduction of IKKα inhibited excessive mitosis, induced terminal differentiation, and prevented skin cancer through repressing an EGFR-driven autocrine loop.Thus, IKKα serves as an innate surveillant.
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