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- W2565996992 abstract "B163 We previously demonstrated that Bcl-2 overexpression enhances the resistance of PC-3 human prostate cancer cells to radiation by inhibiting apoptosis, increasing proliferation and inhibiting angiogenesis. To further elucidate the relationship between Bcl-2 expression and the angiogenic potential of the PC-3-Bcl-2 cell line, we evaluated whether Bcl-2 could be involved in not only tumorigenicity but angiogenesis as well. Bcl-2 overexpressing clone and a control transfected clone were used for in vitro and in vivo experiments. Bcl-2 overexpression enhanced the tumorigenic ability of prostate cancer xenografts, enhanced the expression and secretion of key angiogenic factors which stimulated synthesis of neovasculature (as evident by CD31 immunohistochemical staining). Specifically, the increased angiogenic potential was correlated with increased serum levels of bFGF, IL-8, and MMP-9. In vitro analysis demonstrated Bcl-2 expressing tumors to be resistant to rapamycin induced apoptosis and to secrete bFGF into culture supernatant. Microarray analysis of Bcl-2 expressing PC-3 prostate cancer cells demonstrated increased transcription of genes involved in metabolism, regulators of biologic processes, and transport factors which included interleukins, growth factors, TNF family, and peptidases. These results demonstrate that Bcl-2 overexpression can regulate tumoral angiogenesis. Targeted therapy directed at Bcl-2 expression and angiogenesis may act synergistically to modulate tumor growth. Hence this work validates Bcl-2 role in tumorigenicity and angiogenesis and support our notion that Bcl-2 is an important target in cancer therapy." @default.
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- W2565996992 date "2007-11-01" @default.
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- W2565996992 title "A role for Bcl-2 ongogene in modulating angiogenesis in prostate cancer" @default.
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