title: The effect of a hyposmotic shock and purinergic agonists on K+(Rb+) efflux from cultured human breast cancer cells.
abstract: The effect of a hyposmotic shock and extracellular ATP on the efflux of K(+)(Rb(+)) from human breast cancer cell lines (MDA-MB-231 and MCF-7) has been examined. A hyposmotic shock increased the fractional efflux of K(+)(Rb(+)) from MDA-MB-231 cells via a pathway which was unaffected by Cl(-) replacement. Apamin, charybdotoxin or removing extracellular Ca(2+) had no effect on volume-activated K(+)(Rb(+)) efflux MDA-MB-231 cells. An osmotic shock also stimulated K(+)(Rb(+)) efflux from MCF-7 cells but to a much lesser extent than found with MDA-MB-231 cells. ATP-stimulated K(+)(Rb(+)) efflux from MDA-MB-231 cells in a dose-dependent fashion but had little effect on K(+)(Rb(+)) release from MCF-7 cells. ATP-stimulated K(+)(Rb(+)) efflux was only inhibited slightly by replacing Cl(-) with NO(3)(-). Removal of external Ca(2+) during treatment with ATP reduced the fractional efflux of K(+)(Rb(+)) in a manner suggesting a role for cellular Ca(2+) stores. Charybdotoxin, but neither apamin nor iberiotoxin, inhibited ATP-stimulated K(+)(Rb(+)) release from MDA-MB-231 cells. Suramin inhibited the ATP-activated efflux of K(+)(Rb(+)). UTP also stimulated K(+)(Rb(+)) efflux from MDA-MB-231 cells whereas ADP, AMP and adenosine were without effect. A combination of an osmotic shock and ATP increased the fractional efflux of K(+)(Rb(+)) to a level greater than the sum of the individual treatments. It appears that the hyposmotically-activated and ATP-stimulated K(+) efflux pathways are separate entities. However, there may be a degree of 'crosstalk' between the two pathways.
authors.affiliation: Hannah Research Institute, Ayr, Scotland, UK. gowi@hri.sari.ac.uk
authors.forename: I F
authors.initials: IF
authors.lastname: Gow
authors.forename: J
authors.initials: J
authors.lastname: Thomson
authors.forename: J
authors.initials: J
authors.lastname: Davidson
authors.forename: D B
authors.initials: DB
authors.lastname: Shennan
mesh_terms: D000255:Adenosine Triphosphate / Q000737:chemistry; D001030:Apamin / Q000737:chemistry; D001943:Breast Neoplasms / Q000473:pathology*; D002118:Calcium / Q000378:metabolism; D045744:Cell Line, Tumor; D018999:Charybdotoxin / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005456:Fluorescent Dyes / Q000494:pharmacology; D016257:Fura-2 / Q000494:pharmacology; D006801:Humans; D009995:Osmosis; D010455:Peptides / Q000737:chemistry; D011188:Potassium / Q000737:chemistry; D011960:Receptors, Estrogen / Q000378:metabolism; D011983:Receptors, Purinergic / Q000737:chemistry / Q000378:metabolism*; D012413:Rubidium / Q000737:chemistry; D013050:Spectrometry, Fluorescence; D013498:Suramin / Q000737:chemistry; D013654:Taurine / Q000737:chemistry; D013997:Time Factors
chemical_list: D005456:Fluorescent Dyes; D010455:Peptides; D011960:Receptors, Estrogen; D011983:Receptors, Purinergic; D018999:Charybdotoxin; D013654:Taurine; D001030:Apamin; D013498:Suramin; C064719:iberiotoxin; D000255:Adenosine Triphosphate; D012413:Rubidium; D011188:Potassium; D002118:Calcium; D016257:Fura-2