Cinar, Irfan, Yayla, Muhammed, Celik, Muhammet, Bilen, Arzu, Bayraktutan, ZaferCinar I., Yayla M., Celik M., Bilen A., Bayraktutan Z.Zafer BAYRAKTUTAN, Muhammet ÇELİK, Arzu BİLEN, İrfan ÇINAR, Muhammed YAYLACinar, I, Yayla, M, Celik, M, Bilen, A, Bayraktutan, Z2023-05-092023-05-092020-10-012020-10-012020-10-012020.01.01Bayraktutan, Z., Çeli̇k, M., Bi̇len, A., Çinar, İ., Yayla, M. (2020). Role of Endothelin 1 on Proliferation and Migration of Human MCF-7 Cells. Eurasian Journal of Medicine, 52(3), 277-282https://hdl.handle.net/20.500.12597/15276https://search.trdizin.gov.tr/publication/detail/415514/role-of-endothelin-1-on-proliferation-and-migration-of-human-mcf-7-cellshttps://hdl.handle.net/20.500.12597/7056The aim of this study was to explore the role of endothelin 1 (ET-1) in human breast cancer proliferation and migration and antagonism of endothelin receptor A (ETAR) and endothelin receptor B (ETBR) by using the non-selective dual ETA/ETB receptor antagonist bosentan and determine its anti-proliferative, anti-metastatic, and apoptotic effects demonstrated by nuclear factor kappa B (NF-kB), vascular endothelial growth factor (VEGF), Caspase 3 and Caspase 9 expression on endothelin-induced proliferation of MCF-7 cell line in vitro.A total of 8,000 cells were seeded into e-plates 24 hours after the cells were incubated with or without 10-4 M BOS (1 hour before ET-1 treatment); 10-7, 10-8, and 10-9 M ET-1 for 1-4 days.Whether ET-1 is present or not in the tumor area, bosentan exerts anti-proliferative effect on breast cancer. However, ET-1 and bosentan group showed important inhibitory effect on tumor migration compared to bosentan alone, which can be attributed to increased activity of ET-1 axis in the presence of ET-1. The imbalance among the NF-kB, caspases, and VEGF, which are predictive factors of carcinogenesis significantly improved after bosentan administration.Our study definitely demonstrated ET-1 and its critical role in cancer progression with apoptotic and anti-apoptotic pathways (NF-κB) and VEGF expression, and migration analyses were also performed. The second major finding was that bosentan inhibited ET-1-mediated effects on tumor proliferation and migration.Objective: The aim of this study was to explore the role of endothelin 1 (ET-1) in human breast cancer proliferation and migration and antagonism of endothelin receptor A (ETAR) and endothelin receptor B (ETBR) by using the non-selective dual ETA/ETB receptor antagonist bosentan and determine its anti-proliferative, anti-metastatic, and apoptotic effects demonstrated by nuclear factor kappa B (NF-kB), vascular endothelial growth factor (VEGF), Caspase 3 and Caspase 9 expression on endothelin-induced proliferation of MCF-7 cell line in vitro. Materials and Methods: A total of 8,000 cells were seeded into e-plates 24 hours after the cells were incubated with or without 10-4 M BOS (1 hour before ET-1 treatment); 10-7, 10-8, and 10-9 M ET-1 for 1-4 days. Results: Whether ET-1 is present or not in the tumor area, bosentan exerts anti-proliferative effect on breast cancer. However, ET-1 and bosentan group showed important inhibitory effect on tumor migration compared to bosentan alone, which can be attributed to increased activity of ET-1 axis in the presence of ET-1. The imbalance among the NF-kB, caspases, and VEGF, which are predictive factors of carcinogenesis significantly improved after bosentan administration. Conclusion: Our study definitely demonstrated ET-1 and its critical role in cancer progression with apop-totic and anti-apoptotic pathways (NF-κB) and VEGF expression, and migration analyses were also per-formed. The second major finding was that bosentan inhibited ET-1-mediated effects on tumor proliferation and migration.Objective: The aim of this study was to explore the role of endothelin 1 (ET-1) in human breast cancer proliferation and migration and antagonism of endothelin receptor A (ETAR) and endothelin receptor B (ETBR) by using the non-selective dual ETA/ETB receptor antagonist bosentan and determine its anti-proliferative, anti-metastatic, and apoptotic effects demonstrated by nuclear factor kappa B (NF-kB), vascular endothelial growth factor (VEGF), Caspase 3 and Caspase 9 expression on endothelin-induced proliferation of MCF-7 cell line in vitro.Materials and Methods: A total of 8,000 cells were seeded into e-plates 24 hours after the cells were incubated with or without 10-4 M BOS (1 hour before ET-1 treatment); 10-7, 10-8, and 10-9 M ET-1 for 1-4 days.Results: Whether ET-1 is present or not in the tumor area, bosentan exerts anti-proliferative effect on breast cancer. However, ET-1 and bosentan group showed important inhibitory effect on tumor migration compared to bosentan alone, which can be attributed to increased activity of ET-1 axis in the presence of ET-1. The imbalance among the NF-kB, caspases, and VEGF, which are predictive factors of carcinogenesis significantly improved after bosentan administration.Conclusion: Our study definitely demonstrated ET-1 and its critical role in cancer progression with apoptotic and anti-apoptotic pathways (NF-κB) and VEGF expression, and migration analyses were also performed. The second major finding was that bosentan inhibited ET-1-mediated effects on tumor proliferation and migration.trueinfo:eu-repo/semantics/openAccessBosentanET-1MCF-7cancermetastasisBosentan | Cancer | ET-1 | MCF-7 | MetastasisJournal Article10.5152/eurasianjmed.2020.2003310.5152/eurasianjmed.2020.200332-s2.0-85095442286WOS:00058921670000933209081415514277277282282521308-8742