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Regulation of tumor angiogenesis by EZH2.

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.

SUBMITTER: Lu C 

PROVIDER: S-EPMC2923653 | biostudies-literature | 2010 Aug

REPOSITORIES: biostudies-literature

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Regulation of tumor angiogenesis by EZH2.

Lu Chunhua C   Han Hee Dong HD   Mangala Lingegowda S LS   Ali-Fehmi Rouba R   Newton Christopher S CS   Ozbun Laurent L   Armaiz-Pena Guillermo N GN   Hu Wei W   Stone Rebecca L RL   Munkarah Adnan A   Ravoori Murali K MK   Shahzad Mian M K MM   Lee Jeong-Won JW   Mora Edna E   Langley Robert R RR   Carroll Amy R AR   Matsuo Koji K   Spannuth Whitney A WA   Schmandt Rosemarie R   Jennings Nicholas B NB   Goodman Blake W BW   Jaffe Robert B RB   Nick Alpa M AM   Kim Hye Sun HS   Guven Eylem Ozturk EO   Chen Ya-Huey YH   Li Long-Yuan LY   Hsu Ming-Chuan MC   Coleman Robert L RL   Calin George A GA   Denkbas Emir B EB   Lim Jae Yun JY   Lee Ju-Seog JS   Kundra Vikas V   Birrer Michael J MJ   Hung Mien-Chie MC   Lopez-Berestein Gabriel G   Sood Anil K AK  

Cancer cell 20100801 2

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 inhibit  ...[more]

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