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Cancer Cell. 2010 Aug 9;18(2):185-97. doi: 10.1016/j.ccr.2010.06.016.

Regulation of tumor angiogenesis by EZH2.

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  • 1Department of Gynecologic Oncology, U.T. M.D. Anderson Cancer Center, Houston, TX 77030, USA.

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.

PMID:
20708159
[PubMed - indexed for MEDLINE]
PMCID:
PMC2923653
Free PMC Article

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