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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/4572


    Title: ERK promotes tumorigenesis by inhibiting FOXO3a via MDM2-mediated degradation
    Authors: Jer-Yen Yang;Cong S. Zong;Weiya Xia;Hirohito Yamaguchi;Qingqing Ding;Xiaoming Xie;Jing-Yu Lang;Chien-Chen Lai;Chun-Ju Chang;Wei-Chien Huang;Hsin Huang;Hsu-Ping Kuo;Dung-Fang Lee;Long-Yuan Li;Huang-Chun Lien;Xiaoyun Cheng;King-Jen Chang;Chwan-Deng Hsiao;Fu-Jen Tsai;Chang-Hai Tsai;Aysegul A. Sahin;William J. Muller;Gordon B. Mills;Dihua Yu;Gabriel N. Hortobagyi;Mien-Chie Hung
    Date: 2008-02
    Issue Date: 2009-11-27 13:56:52 (UTC+8)
    Publisher: Asia University
    Abstract: The RAS?ERK pathway is known to play a pivotal role in differentiation, proliferation and tumour progression. Here, we show that ERK downregulates Forkhead box O 3a (FOXO3a) by directly interacting with and phosphorylating FOXO3a at Ser 294, Ser 344 and Ser 425, which consequently promotes cell proliferation and tumorigenesis. The ERK-phosphorylated FOXO3a degrades via an MDM2-mediated ubiquitin-proteasome pathway. However, the non-phosphorylated FOXO3a mutant is resistant to the interaction and degradation by murine double minute 2 (MDM2), thereby resulting in a strong inhibition of cell proliferation and tumorigenicity. Taken together, our study elucidates a novel pathway in cell growth and tumorigenesis through negative regulation of FOXO3a by RAS?ERK and MDM2.
    Relation: NATURE CELL BIOLOGY 10(2):138-148
    Appears in Collections:[生物科技學系] 期刊論文

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