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- W3008148664 abstract "439 Overexpression of vascular endothelial growth factor (VEGF) is associated with angiogenic phenotype and poor prognosis in a variety of human cancers, including breast cancer. However, the precise mechanism underlying VEGF overexpression in breast cancer remains unknown. Previous studies show that signal transducer and activator of transcription 3 (STAT3) is constitutively activated in breast tumors; this activation is significantly associated with aggressive phenotypes of breast cancer. In the present study, we investigated the role of STAT3 activation on VEGF production and tumor angiogenesis in breast tumors both in vitro and in vivo. Transfection with constitutively activated STAT3 increased STAT3 activation, which in turn, enhanced breast metastasis. In contrast, blockade of STAT3 activation by transfection with siRNA for STAT3 suppressed breast tumor growth in animal models. Furthermore, altered STAT3 activity profoundly affected breast tumor angiogenesis in vivo, tumor cell invasion in vitro, and the expression of basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF), and matrix metalloproteinase-2 (MMP-2) in vivo and in vitro. Finally, STAT3 activity transcriptionally regulated the promoter activity of bFGF as well as VEGF and MMP-2 in human cancer cells. These results indicate STAT3 activation plays an important role in the dysregulated expression of bFGF, VEGF and MMP-2 as well as in the angiogenic and invasive processes utilized by cancer cells_all of which contribute to metastasis. Therefore, STAT3 activation may present a novel target in the treatment of human breast cancer." @default.
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- W3008148664 date "2008-05-01" @default.
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- W3008148664 title "STAT3 activation promotes angiogenesis in human breast cancer cells" @default.
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