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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/4630

    Title: IkappaB kinase promotes tumourigenesis through inhibition of Forkhead transcription factor FOXO3a
    Authors: Hu, M. C-T;Lee, D-F.;Xia, W.;Golfman, L.;Ou-Yang, F.;Yang, J-Y.;Zou, Y.;Bao, S.;Hanada, N.;Saso, H.;Kobayashi, R.;Mien-Chie Hung
    Date: 2004-04
    Issue Date: 2009-11-27 13:57:08 (UTC+8)
    Publisher: Asia University
    Abstract: Nuclear exclusion of the forkhead transcription factor FOXO3a by protein kinase Akt contributes to cell survival. We investigated the pathological relationship between phosphoylated-Akt (Akt-p) and FOXO3a in primary tumors. Surprisingly, FOXO3a was found to be excluded from the nuclei of some tumors lacking Akt-p, suggesting an Akt-independent mechanism of regulating FOXO3a localization. We provide evidence for such a mechanism by showing that IkappaB kinase (IKK) physically interacts with, phosphorylates, and inhibits FOXO3a independent of Akt and causes proteolysis of FOXO3a via the Ub-dependent proteasome pathway. Cytoplasmic FOXO3a correlates with expression of IKKbeta or Akt-p in many tumors and associates with poor survival in breast cancer. Further, constitutive expression of IKKbeta promotes cell proliferation and tumorigenesis that can be overridden by FOXO3a. These results suggest the negative regulation of FOXO factors by IKK as a key mechanism for promoting cell growth and tumorigenesis.
    Relation: CELL 117(2):225-237
    Appears in Collections:[生物科技學系] 期刊論文

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