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首页> 外文期刊>Cellular Physiology and Biochemistry >Cell Growth Inhibition, G(2)/M Cell Cycle Arrest, and Apoptosis Induced by Chloroquine in Human Breast Cancer Cell Line Bcap-37
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Cell Growth Inhibition, G(2)/M Cell Cycle Arrest, and Apoptosis Induced by Chloroquine in Human Breast Cancer Cell Line Bcap-37

机译：细胞生长抑制，G（2）/ M细胞周期阻滞和氯喹诱导在人乳腺癌细胞系Bcap-37中诱导凋亡。

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摘要

Chloroquine is an antimalarial drug that has been used in the treatment and prophylaxis of malaria since the 1950s. The present study was undertaken to examine the effects of chloroquine on Bcap-37 human breast cancer cells' growth, cell cycle modulation, apoptosis induction, and associated molecular alterations in vitro. The chloroquine treatment decreased the viability of Bcap-37 cells in a concentration- and time-dependent manner, which correlated with G(2)/M phase cell cycle arrest. The chloroquine-mediated cell cycle arrest was associated with a decrease in protein levels/activity of polo-like kinase 1 (Plk1), phosphorylated cell division cycle 25C (Cdc25C), phosphorylated extracellular signal-regulated kinase 1/2 (ERK 1/2), phosphorylated Akt. The chloroquine-treated Bcap-37 cells exhibited a marked decrease in the level of mitochondrial transmembrane potential (Delta Psi m),which was accompanied by the activation of caspase-3 and cleaved poly(ADP-ribose) polymerase ( PARP). Exposure of Bcap-37 cells to chloroquine also resulted in the induction of spindle abnormalities. In conclusion, the findings in this study suggested that chloroquine might have potential anticancer efficacy, which could be attributed, in part, to its proliferation inhibition and apoptosis induction of cancer cells through modulation of apoptosis and cell cycle-related proteins expressions, down-regulation of mitochondrial transmembrane potential (Delta Psi m), and induction of spindle abnormalities.
机译：氯喹是一种抗疟疾药物，自1950年代以来一直用于治疗和预防疟疾。进行本研究以检查氯喹对Bcap-37人乳腺癌细胞的生长，细胞周期调节，细胞凋亡诱导及相关分子改变的影响。氯喹治疗以浓度和时间依赖性方式降低Bcap-37细胞的活力，这与G（2）/ M期细胞周期停滞有关。氯喹介导的细胞周期停滞与蛋白质水平/ polo样激酶1（Plk1），磷酸化细胞分裂周期25C（Cdc25C），磷酸化细胞外信号调节激酶1/2（ERK 1/2）的活性降低有关），磷酸化的Akt。氯喹处理的Bcap-37细胞的线粒体跨膜电位（ΔPsi m）水平显着降低，并伴有caspase-3的活化和裂解的聚（ADP-核糖）聚合酶（PARP）的活化。 Bcap-37细胞暴露于氯喹也导致纺锤体异常。总之，这项研究的发现表明，氯喹可能具有潜在的抗癌功效，这部分归因于其通过调节细胞凋亡和细胞周期相关蛋白的表达，下调其对癌细胞的增殖抑制和凋亡诱导作用。线粒体跨膜电位（Delta Psi m）的变化和纺锤体异常的诱发。

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