Urotensin-II triggered breast cancer cell proliferation, whereas its receptor antagonists (palosuran, SB657510, and urantide) significantly inhibited proliferation and positively regulated tumor suppressor genes.
Urotensin-II receptor antagonists inhibit proliferation and positively regulate tumor suppressor genes in MCF-7 breast cancer cells, suggesting a potential novel therapeutic target.
p-value: p=<0.0001
Abstract Background Urotensin-II is a powerful vasoconstrictor peptide. Both the peptide and its receptor, GPR14, affect central nervous system, cardiovascular system, and kidney functions. Urotensin-II was found to be involved in the development of many solid organ tumors. The peptide and its receptor have been demonstrated to be present in breast cancer tissue. Moreover, its human plasma level is increased in breast cancer patients. It has also been reported that some cancer patients may have urotensin gene polymorphisms. Antagonists of this peptide receptor with different chemical structures have been produced and studied in different disease models. There are no experimental or clinical studies investigating the effects of urotensin-II receptor antagonists on breast cancer. In this study, MCF-7 cells were grown in an appropriate environment and then plated in wells. WST-8 was used to detect cell proliferation and inhibition effects. The expression levels of the MTA-1, ESR1, Kiss1, UT-II and UTR genes were measured via quantitative RT‒PCR. This study is the first to show the effects of urotensin-II peptide and its receptor antagonists on breast cancer. Results While urotensin-II increased cell proliferation, all the antagonists had inhibitory effects. When the expression of genes affecting the metastasis or suppression of tumor cells was investigated, urotensin-II increased MTA-1 and ESR1 expression and decreased Kiss1 expression. Urotensin-II receptor antagonists reversed these effects. Conclusions As a result, while urotensin-II triggered breast cancer cell proliferation, its receptor antagonists had inhibitory effects on proliferation and positive regulatory effects on tumor suppressor genes. These results suggest that urotensin-II receptor antagonists may provide effective results for breast cancer treatment.
Olukman et al. (Sat,) conducted a other in Breast cancer. Urotensin-II and UTR antagonists (Palosuran, SB657510, Urantide) vs. Control (0.1% DMSO vehicle) was evaluated on Cell proliferation and inhibition (p=<0.0001). Urotensin-II triggered breast cancer cell proliferation, whereas its receptor antagonists (palosuran, SB657510, and urantide) significantly inhibited proliferation and positively regulated tumor suppressor genes.
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