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Regulation of tumor angiogenesis by EZH2

Authors
 Chunhua Lu  ;  Hee Dong Han  ;  Lingegowda S. Mangala  ;  Rouba Ali-Fehmi  ;  Christopher S. Newton  ;  Laurent Ozbun  ;  Guillermo N. Armaiz-Pena  ;  Wei Hu  ;  Rebecca L. Stone  ;  Adnan Munkarah  ;  Murali K. Ravoori  ;  Mian M. K. Shahzad  ;  Jeong-Won Lee  ;  Edna Mora  ;  Robert R. Langley  ;  Amy R. Carroll  ;  Koji Matsuo  ;  Whitney A. Spannuth  ;  Rosemarie Schmandt  ;  Nicholas B. Jennings  ;  Blake W. Goodman  ;  Robert B. Jaffe  ;  Alpa M. Nick  ;  Hye Sun Kim  ;  Eylem Ozturk Guven  ;  Ya-Huey Chen  ;  Long-Yuan Li  ;  Ming-Chuan Hsu  ;  Robert L. Coleman  ;  George A. Calin  ;  Emir B. Denkbas  ;  Jae Yun Lim  ;  Ju-Seog Lee  ;  Vikas Kundra  ;  Michael J. Birrer  ;  Mien-Chie Hung  ;  Gabriel Lopez-Berestein  ;  Anil K. Sood 
Citation
 CANCER CELL, Vol.18(2) : 185-197, 2010 
Journal Title
 CANCER CELL 
ISSN
 1535-6108 
Issue Date
2010
MeSH
Animals ; Base Sequence ; Cell Line, Tumor ; Cell Proliferation ; DNA Methylation ; DNA Primers ; Enhancer of Zeste Homolog 2 Protein ; Female ; Gene Silencing ; Histone-Lysine N-Methyltransferase/genetics ; Histone-Lysine N-Methyltransferase/physiology* ; Immunohistochemistry ; Mice ; Mice, Nude ; Microscopy, Fluorescence ; Neovascularization, Pathologic/physiopathology* ; Ovarian Neoplasms/blood supply* ; Ovarian Neoplasms/pathology ; Polycomb Repressive Complex 2
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.
Files in This Item:
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DOI
10.1016/j.ccr.2010.06.016
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Lim, Jae Yun(임재윤)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/103209
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