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首页> 外文期刊>International journal of hyperthermia: The official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group >Elevated levels of intracellular Ca(2+) and apoptosis in human lung cancer cells given heat-shock.
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Elevated levels of intracellular Ca(2+) and apoptosis in human lung cancer cells given heat-shock.

机译：给予热激后人肺癌细胞内Ca（2+）和细胞凋亡的水平升高。

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The chronological changes in intracellular Ca(2+)concentrations ([Ca(2+)](i)) were analysed during heat-induced apoptosis in human lung cancer cell lines LK-2 (squamous cell carcinoma) and LU65A (large cell carcinoma). In LK-2 cells, increased [Ca(2+)](i) levels were maintained at levels between 250-350 nm 9 h after heat-shock. Treatment with BAPTA, an intracellular Ca(2+) chelator, prior to heat-shock, decreased the frequency of heat-induced apoptosis in LK-2, while thapsigargin, a selective endoplasmic reticulum Ca(2+)-ATPase inhibitor, did not change the number of apoptotic cells, regardless of the presence or absence of Ca(2+)-supplemented medium. In LU65A cells, treatment with BAPTA or thapsigargin did not alter the apoptotic rates. Western blotting demonstrated that, although expression of Bax and Bcl-2 were not changed by heat-shock, p53 expression was elevated in LK-2, but not LU65A cells. Immunohistochemistry showed that p53 was localized predominantly in the cytoplasms of LK-2 cells, suggesting that p53 protein is not functional in LK-2. Heat-shock also elevated activities of caspase-3, -8 and -9 in both cell lines. It is concluded that a temporal increase in [Ca(2+)](i) is the important initiating factor in hyperthermia-induced apoptosis in LK-2 cells and that, in these two lung cancer cell lines, apoptosis may occur through 'cross-talk' between p53-independent mitochondrial and death receptor pathways.
机译：分析了人类肺癌细胞系LK-2（鳞状细胞癌）和LU65A（大细胞癌）热诱导细胞凋亡期间细胞内Ca（2+）浓度（[Ca（2 +）]（i））的时间变化。 ）。在LK-2细胞中，热激后9小时，[Ca（2 +）]（i）的水平保持在250-350 nm之间。用BAPTA，一种在热激之前的细胞内Ca（2+）螯合剂治疗，降低了LK-2中热诱导的细胞凋亡的频率，而thapsigargin，一种选择性内质网Ca（2 +）-ATPase抑制剂，没有改变凋亡细胞的数量，无论是否存在补充Ca（2+）的培养基。在LU65A细胞中，用BAPTA或毒胡萝卜素处理不会改变细胞凋亡率。 Western印迹证实，尽管Bax和Bcl-2的表达没有因热激而改变，但p53表达在LK-2中升高，但在LU65A细胞中没有升高。免疫组织化学显示p53主要位于LK-2细胞的细胞质中，表明p53蛋白在LK-2中不起作用。热激还提高了两种细胞系中caspase-3，-8和-9的活性。结论是，[Ca（2 +）]（i）的暂时增加是热疗诱导LK-2细胞凋亡的重要启动因子，并且在这两种肺癌细胞系中，凋亡可能通过“交叉”发生。 p53独立的线粒体和死亡受体途径之间的“对话”。

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