Journal
CANCER CELL
Volume 18, Issue 2, Pages 185-197Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2010.06.016
Keywords
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Categories
Funding
- NIH [CA 110793, 109298, P50 CA083639, P50 CA098258, CA128797, RC2GM092599]
- Ovarian Cancer Research Fund, Inc
- DOD [OC073399, W81XWH-10-1-0158, BC085265]
- Zarrow Foundation
- Marcus Foundation
- Kim Medlin Fund
- NCI-DHHS-NIH [T32 CA101642]
- GCF/OCRF Ann Schreiber Ovarian Cancer Research
- Meyer and Ida Gordon Foundation
- NIH/NICHD [HD050128]
- GCF-Molly Cade Ovarian Cancer Research
- NSC [97-3111-B-039]
- [NSC-96-3111-B]
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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.
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