ASIA unversity:Item 310904400/16168
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    题名: Regulation of Tumor Angiogenesis by EZH2
    作者: ;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.
    贡献者: 生物科技學系
    关键词: RNA interference;EZH2;chitosan;ovarian carcinoma
    日期: 2010
    上传时间: 2012-11-23 09:09:26 (UTC+0)
    摘要: "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."
    關聯: CANCER CELL
    显示于类别:[生物科技學系] 期刊論文

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