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首页> 外文期刊>Cellular Signalling >Celastrol suppresses breast cancer MCF-7 cell viability via the AMP-activated protein kinase (AMPK)-induced p53-polo like kinase 2 (PLK-2) pathway
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Celastrol suppresses breast cancer MCF-7 cell viability via the AMP-activated protein kinase (AMPK)-induced p53-polo like kinase 2 (PLK-2) pathway

机译：Celastrol通过AMP激活的蛋白激酶（AMPK）诱导的p53-polo like蛋白激酶2（PLK-2）途径抑制乳腺癌MCF-7细胞活力

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摘要

Celastrol, an anti-oxidant flavonoid that is widely distributed in the plant kingdom, has been suggested to have chemopreventive effects on cancer cells: however, the mechanism of this process is not completely understood. In this study, we found that celastrol suppressed the viability of breast cancer MCF-7 cells in an AMP-activated protein kinase (AMPK)-dependent fashion. Celastrol also induced an increase in reactive oxygen species (ROS) levels, leading to AMPK phosphorylation. Protein kinase C (PKC) zeta was also shown to play a role in celastrol-induced ROS generation. In addition, celastrol increased phosphorylation of the pro-apoptotic effector, p53. Inhibition of AMPK blocked celastrol-mediated p53 phosphorylation. Moreover, celastrol increased the expression of tumor suppressor polo like kinase-2 (PLK-2) in a p53-dependent manner. Neither celastrol-induced PLK-2 induction nor celastrol-mediated apoptosis inducing factor poly(ADP-ribose) polymerase-2 (PARP-2) induction was observed in p53 knock-out cells. Furthermore, add-back of PLK-2 resulted in an increase in both celastrol-mediated PARP-2 induction and celastrol-induced apoptotic index sub G1 population. Together, these results suggest that celastrol may have anti-tumor effects on MCF-7 cells via AMPK-induced p53 and PLK-2 pathways.
机译：Celastrol是一种抗氧化剂类黄酮，广泛分布于植物界，已被建议对癌细胞具有化学预防作用：但是，该过程的机制尚未完全明了。在这项研究中，我们发现Celastrol以AMP激活的蛋白激酶（AMPK）依赖性方式抑制了乳腺癌MCF-7细胞的生存能力。 Celastrol还诱导了活性氧（ROS）水平的增加，导致AMPK磷酸化。蛋白激酶C（PKC）zeta也显示在celastrol诱导的ROS产生中起作用。另外，celastrol增加了促凋亡效应子p53的磷酸化。 AMPK的抑制作用可阻断Celastrol介导的p53磷酸化。此外，celastrol以p53依赖性方式增加了肿瘤抑制子polo样激酶2（PLK-2）的表达。在p53基因敲除细胞中未观察到Celastrol诱导的PLK-2诱导或Celastrol介导的凋亡诱导因子聚（ADP-核糖）聚合酶2（PARP-2）诱导。此外，PLK-2的添加导致Celastrol介导的PARP-2诱导和Celastrol诱导的G1细胞凋亡指数的增加。总之，这些结果表明，Celastrol可能通过AMPK诱导的p53和PLK-2途径对MCF-7细胞具有抗肿瘤作用。

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