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M.S., National Taiwan University - 2001
Thesis Advisor: Leroy F. Liu, Ph.D.
Graduate Program in Cellular & Molecular Pharmacology
Pharmacology Department Conference Room
4th floor, RWJMS Research Tower
Monday, April 25, 2011
Increasing evidence has pointed to activated type I interferon signaling in tumors. However, the molecular basis for such activation and its role in tumorigenesis remain unclear. In the current studies, we report that activation of type I interferon (IFN) signaling in tumor cells is due to elevated expression of the type I interferon, IFN-ƒÒ. Further studies in oncogene-transformed cells have suggested that oncogenes such as Ras and Src can activate type I interferon signaling through elevated expression of IFN-£]. Most significantly, IFN-£] autocrine signaling in Ras-transformed mammary epithelial MCF-10A cells was shown to promote Ras transformation and cell invasiveness. Our results demonstrate for the first time that the type I IFN, IFN-£], promotes Ras transformation and cell invasiveness through autocrine signaling, and supports the notion that oncogene-induced cytokines play important roles in transformation and tumorigenesis.