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- W3205413721 abstract "2063 The vasoactive peptide ET-1 has been implicated in the progression of prostate and other cancers. To explore this further, we generated prostate cancer cell lines (PC-3 and 22Rv1) overexpressing ET-1 from a retroviral vector. Using this approach, we achieved 127- and 88-fold overexpression of ET-1 in PC-3 and 22Rv1 cells, respectively, compared to vector controls. This level of ET-1 secretion was comparable to that secreted by primary human lung microvascular endothelial cells. Overexpression of ET-1 leads to a modest increase in PC-3 cell growth in vitro (~2 fold). This occurred through an endothelin receptor A (ETA)-dependent autocrine mechanism. ET-1 overexpression did not affect growth of ETA-deficient 22Rv1 cells. Surprisingly, both 22Rv1 and PC-3 ET-1 overexpressing cells produced significantly smaller subcutaneous tumors compared to controls. Furthermore 22Rv1 ET-1 overexpressing cells delivered via intracardiac route failed to grow in liver, adrenal gland, or bone though viable tumor cells did colonize these organs as assessed by bioluminescence imaging. Based on these data, wehypothesized that overexpression of ET-1 may have an effect on the tumor microenvironment that inhibits tumor growth. Initially, we investigated angiogenesis in PC-3 and 22Rv1 ET-1 overexpressing subcutaneous tumors. We determined that PC-3 ET-1 overexpressing tumors demonstrated decreased microvessel density (MVD) and vascular endothelial growth factor (VEGF) expression compared to vector control. However, 22Rv1 ET-1 overexpressing tumors did not exhibit alterations in MVD or VEGF expression compared to controls suggesting other mechanisms are involved in poor tumor growth. Indeed, preliminary microCT analysis following Microfil resin infusion suggested vasoconstriction of tumor-feeding arterioles within and near the ET-1 overexpressing tumors. Furthermore, growth of subcutaneous ET-1 overexpressing tumors was partially restored by an orally administered systemic vasodilator, hydralazine. Taken together, these data suggest that localized ET-1 concentration in vivo is critical for determining the balance between suppression of tumor growth (vasoconstriction) and growth promotion (mitogenesis and angiogenesis)." @default.
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- W3205413721 date "2008-05-01" @default.
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- W3205413721 title "Endothelin-1 overexpression inhibits prostate cancer growth in vivo through vasoconstriction of tumor-feeding arterioles" @default.
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