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• W2015672145 abstract "BACKGROUND 2-Methoxyestradiol (2ME2) is an antitumoral and antiangiogenic compound that inhibits hypoxia-inducible factor (HIF)-1, a key regulator of the hypoxic response that promotes tumor progression. HIF-1α, the regulated subunit of HIF-1, is overexpressed in premalignant, cancerous and metastatic lesions of prostate. Endothelin (ET)-1 is a HIF target gene and one that plays an important role during prostate bone metastasis via its interaction with endothelin A (ETA) receptor. We reasoned that 2ME2 combined with an ETA receptor antagonist would induce potent cytotoxic effects in prostate cancer cells. METHODS PC-3 and LNCaP cells were grown alone or cocultured with human osteoblasts. The cells were treated with 2ME2, with an ETA receptor antagonist (BQ-123) or with combinations of both compounds. The cells were then evaluated for cytotoxicity, HIF-1α protein expression and HIF-1 transcriptional activity. RESULTS The combination of 2ME2 with BQ-123 induced synergistic cytotoxic effects in prostate cancer cells and in their cocultures with osteoblasts. No synergism was observed when 2ME2 was combined with the ETB selective antagonist, BQ-788. These results correlated with inhibition of HIF-1α protein expression, HIF-1 transcriptional activity, and PSA mRNA expression. CONCLUSIONS The ETA receptor antagonist was capable of potentiating the cytotoxic effects of 2ME2 in prostate cancer cells. These effects were apparently mediated through the inhibition of the HIF-1 pathway. Our in vitro data strengthen the rationale for using 2ME2 in combination with ETA receptor antagonists for the treatment of metastatic prostate cancer. Prostate 68: 679–689, 2008. © 2008 Wiley-Liss, Inc." @default.
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• W2015672145 date "2008-05-01" @default.
• W2015672145 modified "2023-09-27" @default.
• W2015672145 title "Potentiation of 2-Methoxyestradiol-Induced cytotoxicity by blocking endothelin A receptor in prostate cancer cells" @default.
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• W2015672145 doi "https://doi.org/10.1002/pros.20734" @default.
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