title: Effect of m-3M3FBS on Ca²⁺ movement in PC3 human prostate cancer cells.
abstract: The effect of 2,4,6-trimethyl-N-(meta-3-trifluoromethyl-phenyl)-benzenesulfonamide (m-3M3FBS), a presumed phospholipase C activator, on cytosolic free Ca²⁺ concentrations ([Ca²⁺]i) in PC3 human prostate cancer cells is unclear. This study explored whether m-3M3FBS changed basal [Ca²⁺]i levels in suspended PC3 cells by using fura-2 as a Ca²⁺-sensitive fluorescent dye. M-3M3FBS at concentrations between 10-50 microM increased [Ca²⁺]i in a concentration-dependent manner. The Ca²⁺ signal was reduced by 60% by removing extracellular Ca²⁺. M-3M3FBS-induced Ca²⁺ influx was inhibited by the store-operated Ca²⁺ channel blockers nifedipine, econazole and SK&F96365, and by the phospholipase A2 inhibitor aristolochic acid. In Ca²⁺-free medium, 30 microM m-3M3FBS pretreatment greatly inhibited the [Ca²⁺]i rise induced by the endoplasmic reticulum Ca²⁺ pump inhibitor thapsigargin or BHQ. Conversely, pretreatment with thapsigargin, BHQ or cyclopiazonic acid reduced the major part of m-3M3FBS-induced [Ca²⁺]i rise. Inhibition of phospholipase C with U73122 did not much alter m-3M3FBS-induced [Ca²⁺]i rise. Collectively, in PC3 cells, m-3M3FBS induced [Ca²⁺]i rises by causing phospholipase C-independent Ca²⁺ release from the endoplasmic reticulum and Ca²⁺ influx via store-operated Ca²⁺ channels.
authors.affiliation: Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung 81362, Taiwan, Republic of China.
authors.forename: Jeng-Yu
authors.initials: JY
authors.lastname: Tsai
authors.forename: Pochuen
authors.initials: P
authors.lastname: Shieh
authors.forename: Daih-Huang
authors.initials: DH
authors.lastname: Kuo
authors.forename: Fu-An
authors.initials: FA
authors.lastname: Chen
authors.forename: Chun-Chi
authors.initials: CC
authors.lastname: Kuo
authors.forename: Chung-Ren
authors.initials: CR
authors.lastname: Jan
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism* / Q000473:pathology; D034341:Aristolochic Acids / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020013:Calcium Signaling / Q000187:drug effects* / Q000502:physiology; D045744:Cell Line, Tumor; D004305:Dose-Response Relationship, Drug; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D006801:Humans; D007211:Indoles / Q000494:pharmacology; D008297:Male; D023421:Models, Animal; D064801:Phospholipase A2 Inhibitors; D011471:Prostatic Neoplasms / Q000378:metabolism* / Q000473:pathology; D013449:Sulfonamides / Q000494:pharmacology*; D019284:Thapsigargin / Q000494:pharmacology; D010738:Type C Phospholipases / Q000378:metabolism; D000096926:Benzenesulfonamides
chemical_list: D034341:Aristolochic Acids; D002118:Calcium; D002121:Calcium Channel Blockers; D007211:Indoles; D064801:Phospholipase A2 Inhibitors; D013449:Sulfonamides; D019284:Thapsigargin; D010738:Type C Phospholipases; C473783:2,4,6-trimethyl-N-(meta-3-trifluoromethylphenyl)benzenesulfonamide; D000096926:Benzenesulfonamides; C000228:aristolochic acid I; C000543:cyclopiazonic acid