title: Capacitative calcium influx in human epithelial breast cancer and non-tumorigenic cells occurs through Ca2+ entry pathways with different permeabilities to divalent cations.
abstract: The operation of capacitative Ca(2+) entry (CCE) in human breast cancer (SKBR3) and non-tumorigenic (HBL100) cell lines was investigated as an alternative Ca(2+) entry route in these cells. Ca(2+) readdition after thapsigargin-induced store depletion showed activation of CCE in both cell lines. SKBR3 cells exhibited retarded store depletion and CCE decay kinetics compared to the non-tumorigenic HBL100 cells, suggesting alterations in Ca(2+) homeostasis. CCE was also highly permeable to Mn(2+) and to a lesser extent to Sr(2+), but not to Ba(2+). In HBL100 cells, CCE is contributed (30%) by a Ca(2+)/Mn(2+) permeable route insensitive to low (1 microM) Gd(3+) and a Ca(2+)/Sr(2+)/Mn(2+) permeable non-selective pathway (70%) sensitive to 1 microM Gd(3+). In SKBR3 cells, the relative contribution to CCE of both routes was opposite to that in non-tumorigenic cells.
authors.affiliation: Departamento de Biología, Bioquímica y Farmacia, Universidad Nacional del Sur San Juan 670, (8000) Bahía Blanca, Argentina.
authors.forename: Carolina
authors.initials: C
authors.lastname: Baldi
authors.forename: Guillermo
authors.initials: G
authors.lastname: Vazquez
authors.forename: Ricardo
authors.initials: R
authors.lastname: Boland
mesh_terms: D001943:Breast Neoplasms / Q000503:physiopathology*; D002118:Calcium / Q000032:analysis / Q000378:metabolism*; D002273:Carcinogens; D002413:Cations, Divalent; D002460:Cell Line; D002463:Cell Membrane Permeability / Q000502:physiology; D004791:Enzyme Inhibitors; D004847:Epithelial Cells / Q000378:metabolism / Q000502:physiology; D006801:Humans; D007473:Ion Channels / Q000378:metabolism*; D019284:Thapsigargin; D014407:Tumor Cells, Cultured
chemical_list: D002273:Carcinogens; D002413:Cations, Divalent; D004791:Enzyme Inhibitors; D007473:Ion Channels; D019284:Thapsigargin; D002118:Calcium