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題名 | Rise of [Ca²⁺]ᵢ and Apoptosis Induced by M-3M3FBS in SCM1 Human Gastric Cancer Cells= |
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作者 | Chen, Wei-chuan; Chou, Chiang-ting; Liou, Wen-chin; Liu, Shiuh-inn; Lin, Ko-long; Lu, Ti; Lu, Yi-chau; Hsu, Shu-shong; Tsai, Jeng-yu; Liao, Wei-chuan; Liang, Wei-zhe; Jan, Chung-ren; |
期刊 | The Chinese Journal of Physiology |
出版日期 | 20140200 |
卷期 | 57:1 2014.02[民103.02] |
頁次 | 頁31-40 |
分類號 | 415.138 |
語文 | eng |
關鍵詞 | Apoptosis; Ca²⁺; m-3M3FBS; SCM1; |
英文摘要 | M-3M3FBS (2,4,6-trimethyl-N-(meta-3-trifluoromethyl-phenyl)-benzenesulfonamide is a presumed phospholipase C activator which induced Ca2+ movement and apoptosis in different cell models. However, the effect of m-3M3FBS on cytosolic free Ca2+ concentrations ([Ca2+]i ) and apoptosis in SCM1 human gastric cancer cells is unclear. This study explored whether m-3M3FBS elevated basal [Ca2+]i levels in suspended cells by using fura-2 as a Ca2+-sensitive fluorescent dye. M-3M3FBS at concentrations between 5-50 µM increased [Ca2+]i in a concentration-dependent manner. The Ca2+ signal was reduced by half by removing extracellular Ca2+. M-3M3FBS-induced Ca2+ influx was inhibited by nifedipine, econazole, SK&F96365, aristolochic acid, and GF109203X. In Ca2+-free medium, 50 µM m-3M3FBS pretreatment inhibited the [Ca2+]i rise induced by the endoplasmic reticulum Ca2+ pump inhibitor thapsigargin. Conversely, pretreatment with thapsigargin partly reduced m-3M3FBS-induced [Ca2+]i rise. Suppression of inositol 1,4,5-trisphosphate production with U73122 did not change m-3M3FBSinduced [Ca2+]i rise. At concentrations between 25 and 50 µM m-3M3FBS killed cells in a concentrationdependent manner. The cytotoxic effect of m-3M3FBS was not reversed by prechelating cytosolic Ca2+ with acetoxy-methyl ester of bis-(o-aminophenoxy)-ethane-N,N,N’,N’-tetraacetic acid (BAPTA/AM). Annexin V/propidium iodide staining data suggest that m-3M3FBS induced apoptosis at 25 and 50 µM. M-3M3FBS also increased levels of superoxide. Together, in human gastric cancer cells, m-3M3FBS induced a [Ca2+]i rise by inducing phospholipase C-independent Ca2+ release from the endoplasmic reticulum and Ca2+ entry via protein kinase C-sensitive store-operated Ca2+ channels. M-3M3FBS induced cell death that might involve apoptosis via reactive oxygen species production. |
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