α2-adrenergic effect on human breast cancer MCF-7 cells
(-)Epinephrine (Epi) and (-)Norepinephrine (NEpi) significantly stimulated tritiated Thymidine incorporation in MCF-7 cells at concentrations 10-30 pM to 10 nM, with an EC50 of 10 pM for Epi and 14.2 pM for NEpi. To characterize this action, cells were incubated in the presence of NEpi or Epi and di...
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1999
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01676806_v55_n1_p41_Vazquez http://hdl.handle.net/20.500.12110/paper_01676806_v55_n1_p41_Vazquez |
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paper:paper_01676806_v55_n1_p41_Vazquez2023-06-08T15:16:44Z α2-adrenergic effect on human breast cancer MCF-7 cells α2-adrenergic agonists α2-adrenergic antagonists α2-adrenoceptor Breast cancer Catecholamines Human adrenalin alpha 2 adrenergic receptor cyclic AMP noradrenalin phentolamine prazosin propranolol yohimbine adrenalin alpha adrenergic receptor blocking agent alpha adrenergic receptor stimulating agent beta adrenergic receptor blocking agent clonidine cyclic AMP noradrenalin phentolamine prazosin propranolol yohimbine article breast cancer cancer cell culture cell stimulation concentration response controlled study DNA synthesis human human cell priority journal breast tumor cell culture cell division drug antagonism drug effect female metabolism pathology physiology Adrenergic alpha-Agonists Adrenergic alpha-Antagonists Adrenergic beta-Antagonists Breast Neoplasms Cell Division Cells, Cultured Clonidine Cyclic AMP Epinephrine Female Humans Norepinephrine Phentolamine Prazosin Propranolol Tumor Cells, Cultured Yohimbine (-)Epinephrine (Epi) and (-)Norepinephrine (NEpi) significantly stimulated tritiated Thymidine incorporation in MCF-7 cells at concentrations 10-30 pM to 10 nM, with an EC50 of 10 pM for Epi and 14.2 pM for NEpi. To characterize this action, cells were incubated in the presence of NEpi or Epi and different antagonists. The β-adrenergic antagonist Propanolol showed no effect on the agonist's stimulation, whereas the α-adrenergic antagonist Phentolamine, reverted it completely at high concentrations (100 μM). The α1-adrenergic antagonist Prazosin (Pra) acted only at high concentrations, while the α2-adrenergic antagonist Yohimbine (Yo) reverted the stimulation at an EC50 of 0.11 μM. Likewise, when the cells were incubated in the presence of the specific α2-adrenergic agonist Clonidine (Clo), Thymidine incorporation was significantly stimulated at an EC50 of 0.298 pM. Again, the incubation of the cells in the presence of the α1-adrenergic antagonist Pra exerted its action at high concentrations, whereas the α2-adrenergic antagonist Yo showed a clear reversal of the agonist's enhancement at an EC50 of 0.136 μM. Moreover, Clo caused a clear and significant inhibition of stimulated cAMP levels both in the intracellular and the extracellular fractions. Yo showed a complete reversion of cAMP levels to control values in the presence of Clo, while Pra had the opposite effect. These data suggest that the stimulation provoked in Thymidine incorporation by the agonists Epi, NEpi, and Clo is, at least in part, due to an α2-adrenergic mechanism directly on tumoral cells, and that the effect is coupled with inhibition of cAMP levels, as described for this kind of receptors. 1999 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01676806_v55_n1_p41_Vazquez http://hdl.handle.net/20.500.12110/paper_01676806_v55_n1_p41_Vazquez |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
α2-adrenergic agonists α2-adrenergic antagonists α2-adrenoceptor Breast cancer Catecholamines Human adrenalin alpha 2 adrenergic receptor cyclic AMP noradrenalin phentolamine prazosin propranolol yohimbine adrenalin alpha adrenergic receptor blocking agent alpha adrenergic receptor stimulating agent beta adrenergic receptor blocking agent clonidine cyclic AMP noradrenalin phentolamine prazosin propranolol yohimbine article breast cancer cancer cell culture cell stimulation concentration response controlled study DNA synthesis human human cell priority journal breast tumor cell culture cell division drug antagonism drug effect female metabolism pathology physiology Adrenergic alpha-Agonists Adrenergic alpha-Antagonists Adrenergic beta-Antagonists Breast Neoplasms Cell Division Cells, Cultured Clonidine Cyclic AMP Epinephrine Female Humans Norepinephrine Phentolamine Prazosin Propranolol Tumor Cells, Cultured Yohimbine |
| spellingShingle |
α2-adrenergic agonists α2-adrenergic antagonists α2-adrenoceptor Breast cancer Catecholamines Human adrenalin alpha 2 adrenergic receptor cyclic AMP noradrenalin phentolamine prazosin propranolol yohimbine adrenalin alpha adrenergic receptor blocking agent alpha adrenergic receptor stimulating agent beta adrenergic receptor blocking agent clonidine cyclic AMP noradrenalin phentolamine prazosin propranolol yohimbine article breast cancer cancer cell culture cell stimulation concentration response controlled study DNA synthesis human human cell priority journal breast tumor cell culture cell division drug antagonism drug effect female metabolism pathology physiology Adrenergic alpha-Agonists Adrenergic alpha-Antagonists Adrenergic beta-Antagonists Breast Neoplasms Cell Division Cells, Cultured Clonidine Cyclic AMP Epinephrine Female Humans Norepinephrine Phentolamine Prazosin Propranolol Tumor Cells, Cultured Yohimbine α2-adrenergic effect on human breast cancer MCF-7 cells |
| topic_facet |
α2-adrenergic agonists α2-adrenergic antagonists α2-adrenoceptor Breast cancer Catecholamines Human adrenalin alpha 2 adrenergic receptor cyclic AMP noradrenalin phentolamine prazosin propranolol yohimbine adrenalin alpha adrenergic receptor blocking agent alpha adrenergic receptor stimulating agent beta adrenergic receptor blocking agent clonidine cyclic AMP noradrenalin phentolamine prazosin propranolol yohimbine article breast cancer cancer cell culture cell stimulation concentration response controlled study DNA synthesis human human cell priority journal breast tumor cell culture cell division drug antagonism drug effect female metabolism pathology physiology Adrenergic alpha-Agonists Adrenergic alpha-Antagonists Adrenergic beta-Antagonists Breast Neoplasms Cell Division Cells, Cultured Clonidine Cyclic AMP Epinephrine Female Humans Norepinephrine Phentolamine Prazosin Propranolol Tumor Cells, Cultured Yohimbine |
| description |
(-)Epinephrine (Epi) and (-)Norepinephrine (NEpi) significantly stimulated tritiated Thymidine incorporation in MCF-7 cells at concentrations 10-30 pM to 10 nM, with an EC50 of 10 pM for Epi and 14.2 pM for NEpi. To characterize this action, cells were incubated in the presence of NEpi or Epi and different antagonists. The β-adrenergic antagonist Propanolol showed no effect on the agonist's stimulation, whereas the α-adrenergic antagonist Phentolamine, reverted it completely at high concentrations (100 μM). The α1-adrenergic antagonist Prazosin (Pra) acted only at high concentrations, while the α2-adrenergic antagonist Yohimbine (Yo) reverted the stimulation at an EC50 of 0.11 μM. Likewise, when the cells were incubated in the presence of the specific α2-adrenergic agonist Clonidine (Clo), Thymidine incorporation was significantly stimulated at an EC50 of 0.298 pM. Again, the incubation of the cells in the presence of the α1-adrenergic antagonist Pra exerted its action at high concentrations, whereas the α2-adrenergic antagonist Yo showed a clear reversal of the agonist's enhancement at an EC50 of 0.136 μM. Moreover, Clo caused a clear and significant inhibition of stimulated cAMP levels both in the intracellular and the extracellular fractions. Yo showed a complete reversion of cAMP levels to control values in the presence of Clo, while Pra had the opposite effect. These data suggest that the stimulation provoked in Thymidine incorporation by the agonists Epi, NEpi, and Clo is, at least in part, due to an α2-adrenergic mechanism directly on tumoral cells, and that the effect is coupled with inhibition of cAMP levels, as described for this kind of receptors. |
| title |
α2-adrenergic effect on human breast cancer MCF-7 cells |
| title_short |
α2-adrenergic effect on human breast cancer MCF-7 cells |
| title_full |
α2-adrenergic effect on human breast cancer MCF-7 cells |
| title_fullStr |
α2-adrenergic effect on human breast cancer MCF-7 cells |
| title_full_unstemmed |
α2-adrenergic effect on human breast cancer MCF-7 cells |
| title_sort |
α2-adrenergic effect on human breast cancer mcf-7 cells |
| publishDate |
1999 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_01676806_v55_n1_p41_Vazquez http://hdl.handle.net/20.500.12110/paper_01676806_v55_n1_p41_Vazquez |
| _version_ |
1768543653513396224 |