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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/16168


    Title: Regulation of Tumor Angiogenesis by EZH2
    Authors: ;Lu, C.;Han, H.D.;Mangala, L.S.;Ali-Fehmi, R.;Newton, C.;Ozbun, L;Armaiz-Pena, G.;Hu, W.;Stone, R;Munkarah, A;Ravoori, M.K.;Shahzad, M.;Lee, J.W.;Mora.E.;Langley, R.R.;Carroll, A.R.;Matsuo, K.;Spannuth, W.A.;Schmandt, R.;Jennings, N.B;Goodman, B.W.;Jaffe, R.B.;Nick, A.M.;Kim, H.S.;Guven, E.O.;Chen, Y.H.;李龍緣;Li, Long-Yuan;Hsu, M.C.;Coleman, R.L.;Calin, G.A.;Denkbas, E.B.;Lim, J.Y.;Lee, J.S.;Kundra, V.;Birrer, M.J;洪明奇;Hung, Mien-Chie;Lopez-Berestein, G;Sood, A,K.
    Contributors: 生物科技學系
    Keywords: RNA interference;EZH2;chitosan;ovarian carcinoma
    Date: 2010
    Issue Date: 2012-11-23 17:09:26 (UTC+8)
    Abstract: "Although VEGF-targeted therapies are showing promise, new angiogenesis targets are needed to make additional gains. Here, we show that increased Zeste homolog 2 (EZH2) expression in either tumor cells or in tumor vasculature is predictive of poor clinical outcome. The increase in endothelial EZH2 is a direct result of VEGF stimulation by a paracrine circuit that promotes angiogenesis by methylating and silencing vasohibin1 (vash1). Ezh2 silencing in the tumor-associated endothelial cells inhibited angiogenesis mediated by reactivation of VASH1, and reduced ovarian cancer growth, which is further enhanced in combination with ezh2 silencing in tumor cells. Collectively, these data support the potential for targeting ezh2 as an important therapeutic approach.
    2010 Elsevier Inc. All rights reserved."
    Relation: CANCER CELL
    Appears in Collections:[生物科技學系] 期刊論文

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