...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of Cellular Physiology >Inhibition of ATP-sensitive potassium channels causes reversible cell-cycle arrest of human breast cancer cells in tissue culture.
【24h】

Inhibition of ATP-sensitive potassium channels causes reversible cell-cycle arrest of human breast cancer cells in tissue culture.

机译：抑制ATP-sensitive钾离子通道使可逆细胞循环逮捕的人类乳腺癌细胞在组织文化。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The purpose of this study was to determine if potassium channel activity is required for the proliferation of MCF-7 human mammary carcinoma cells. We examined the sensitivities of proliferation and progress through the cell cycle to each of nine potassium channel antagonists. Five of the potassium channel antagonists produced a concentration-dependent inhibition of cell proliferation with no evidence of cytotoxicity following a 3-day or 5-day exposure to drug. The IC50 values for these five drugs, quinidine (25 microM), glibenclamide (50 microM), linogliride (770 microM), 4-aminopyridine (1.6 mM), and tetraethylammonium (5.8 mM) were estimated from their respective concentration-response curves. Four other potassium channel blockers were tested at supra-maximal channel blocking concentrations, including charybdotoxin (200 nM), iberiotoxin (100 nM), margatoxin (10 nM), and apamin (500 nM), and they had no effect on MCF-7 cell proliferation, viability, or cell cycle distribution. Of the five drugs that inhibited proliferation, only quinidine, glibenclamide, and linogliride also affected the cell cycle distribution. Cell populations exposed to each of these drugs for 3 days showed a statistically significant accumulation in G0/G1 phase and a significant proportional reduction in S phase and G2/M phase cells. The inhibition of cell proliferation correlated significantly with the extent of cell accumulation in G0/G1 phase and the threshold concentrations for inhibition of growth and G0/G1 arrest were similar. The G0/G1 arrest produced by quinidine and glibenclamide were reversed by removing the drug, and cells released from arrest entered S phase synchronously with a lag period of approximately 24 hours. Based on the differential sensitivity of cell proliferation and cell cycle progression to the nine potassium channel antagonists, we conclude that inhibition of ATP-sensitive potassium channels in these human mammary carcinoma cells, reversibly arrests the cells in the G0/G1 phase of the cell cycle, resulting in an inhibition of cell proliferation.
机译：本研究的目的是确定钾通道所需的活动MCF-7人类乳房癌扩散细胞。通过细胞周期增殖和进步每个九钾通道拮抗剂。五的钾离子通道拮抗剂的浓度抑制生产没有证据表明细胞增殖细胞毒性为期3天或5天之后出现的风险药物。奎尼丁(25 microM)、格列本脲(50 microM),linogliride (770 microM), 4-aminopyridine (1.6毫米),四乙铵(5.8毫米)估计从各自的量效曲线。钾通道阻滞剂进行测试supra-maximal通道阻塞的浓度,iberiotoxin包括charybdotoxin(200海里)(100海里),margatoxin(10海里),和apamin (500海里),他们对MCF-7细胞没有影响增殖、生存能力或细胞周期分布。扩散,只有奎尼丁、格列本脲和linogliride也对细胞周期的影响分布。这些药物3天显示统计重要的积累在G0 / G1期显著减少S期和成比例G2 / M期细胞。与扩散显著相关程度的细胞G0 / G1期和积累为抑制阈值浓度增长和G0 / G1逮捕是相同的。逮捕由奎尼丁和格列本脲被删除逆转药物,细胞释放被捕进入S期同步与约的滞后期24小时。细胞增殖和细胞周期的进展九个钾离子通道拮抗剂,我们得出结论:ATP-sensitive抑制钾离子通道在这些人类乳腺癌的细胞,可逆地逮捕的细胞G0 / G1期细胞周期,导致细胞增殖的抑制作用。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号