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• W3044689586 abstract "1290 Angiogenesis or the formation of new blood vessels is essential for tumor expansion, and vascular endothelial growth factor (VEGF) is one of the most potent angiogenic growth factors known. We recently discovered that natural and synthetic progestins induce VEGF in a sub-set of breast cancer cells in a progesterone receptor (PR) dependent manner. This observation could be very significant since a vast majority of all breast tumors are estrogen receptor and PR-positive. It is known that tumor-secreted VEGF can diffuse from tumor cells and increase the proliferation of surrounding endothelial cells. However, it is not known if hormone-induced VEGF from tumor cells can also regulate angiogenesis, thereby leading to tissue expansion. It is thus critical to investigate the functional role of progestin-induced VEGF in promoting angiogenesis and breast cancer cell growth, since PR could be considered a target for therapeutic intervention of VEGF production. In the present study, we investigated whether progestin-induced VEGF from breast tumor cell lines can function in a paracrine manner to induce proliferation of endothelial cells, and in addition if hormone induced VEGF can function in a paracrine/autocrine manner to increase the proliferation of tumor epithelial cells. Our novel findings indicate that conditioned medium from a sub-set of progestin-treated breast tumor cells can induce proliferation of endothelial cells in a paracrine manner and can induce proliferation of tumor epithelial cells in a paracrine and an autocrine manner. The use of an anti-VEGF antibody and SU-1498, an inhibitor of the VEGF receptor-2 (VEGFR-2 or flk/kdr) demonstrated that these proliferative effects involve interactions between VEGF and VEGFR-2. Also, blockage of progestin-induced VEGF by the anti-progestin RU-486 eliminated VEGF-induced proliferative effects. The ability of VEGF to increase proliferation of endothelial cells and tumor cells, including tumor cells that do not release VEGF in response to progestins, suggests that these effects are mediated by amplification of the progestin signal, which ultimately results in angiogenesis and tumor growth. These novel findings suggest that targeting the release of VEGF from tumor epithelial cells and blocking interactions between VEGF and VEGFR-2 on both endothelial and tumor epithelial cells may lead to the development of new anti-angiogenic therapies for progestin-dependent breast tumors. Furthermore, these data indicate that PR is a molecular target for anti-angiogenic therapy and that selective PR modulators should be developed to block release of angiogenic growth factors from the breast cancer cells. Supported by NIH grant CA-86916. SMH is the Zalk Missouri Professor of Tumor Angiogenesis." @default.
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• W3044689586 date "2005-05-01" @default.
• W3044689586 modified "2023-09-26" @default.
• W3044689586 title "Proliferation of Endothelial and Tumor Epithelial Cells by Progestin- Induced VEGF from Human Breast Cancer Cells: Paracrine and Autocrine Effects" @default.
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