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首页> 外文期刊>Journal of Cellular Physiology >Coumestrol Inhibits Proliferation and Migration of Prostate Cancer Cells by Regulating AKT, ERK1/2, and JNK MAPK Cell Signaling Cascades
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Coumestrol Inhibits Proliferation and Migration of Prostate Cancer Cells by Regulating AKT, ERK1/2, and JNK MAPK Cell Signaling Cascades

机译:Coumestrol抑制增殖和迁移ERK1/2前列腺癌细胞通过调节一种蛋白激酶,和物细胞MAPK信号级联

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Coumestrol is the one of the major phytoestrogens which is abundant in soybeans, legumes, brussel sprouts, and spinach. The beneficial effects of coumestrol are well known in various biological processes including; neuroprotective effects on the nervous system, function of the female reproductive system, anti-bacterial properties, and anti-cancer effects. Although the anti-tumor activity of coumestrol has been demonstrated for ovarian, breast, lung, and cervical cancers, little is known of its effects on prostate cancer. Therefore, in the present study, we investigated the chemotherapeutic effects of coumestrol on two prostate cancer cell lines, PC3 and LNCaP. Our results showed that coumestrol decreased proliferation and migration and induced apoptosis in both PC3 and LNCaP cells. Moreover, effects of coumestrol on cell signaling pathways were investigated and it increased phosphorylation of ERK1/2, JNK, P90RSK, and P53 proteins in a dose- and time-dependent manner whereas phosphorylation of AKT was reduced by coumestrol under the same conditions for culture of PC3 and LNCaP cells. In addition, mitochondrial dysfunction was induced by coumestrol as evidenced by a significant loss of mitochondrial membrane potential. Furthermore, cleavage of caspase-3 and caspase-9, the apoptotic proteins associated with mitochondria, also changed in response to coumestrol. Coumestrol also caused mitochondrial dysfunction resulting in an increase in ROS production in PC3 and LNCaP cells. These results suggest that coumestrol can inhibit progression of prostate cancer and may be a novel chemotherapeutic agent for treatment of prostate cancer via effects mediated via the PI3K/AKT and ERK1/2 and JNK MAPK cell signaling pathways. J. Cell. Physiol. 232: 862-871, 2017. (c) 2016 Wiley Periodicals, Inc.
机译:Coumestrol是主要的植物雌激素丰富的大豆,豆类,布鲁塞尔豆芽、菠菜。在各种生物coumestrol是众所周知的过程包括;女性的神经系统功能生殖系统、抗菌性能和抗癌效果。活动coumestrol已经证明了的卵巢癌、乳腺癌、肺癌、宫颈癌,对前列腺的影响所知甚少癌症。调查的化疗效果coumestrol前列腺癌在两个细胞系,生物和LNCaP。减少扩散和迁移和诱导在生物和LNCaP细胞凋亡。coumestrol对细胞信号通路的影响进行调查和增加吗磷酸化ERK1/2、物、P90RSK和P53蛋白质剂量和时间的方式而一种蛋白激酶的磷酸化是减少了coumestrol在相同条件下的文化,生物和LNCaP细胞。线粒体功能障碍引起的coumestrol就是明证的重大损失线粒体膜电位。乳沟caspase-3 caspase-9,凋亡与线粒体相关的蛋白质,在应对coumestrol也改变了。Coumestrol还导致线粒体功能障碍导致生物活性氧产量的增加和LNCaP细胞。coumestrol可以抑制前列腺癌的进展癌症和可能是一个新颖的化学治疗剂通过影响前列腺癌的治疗通过PI3K / AKT介导和ERK1/2物MAPK细胞信号通路。862 - 871年,2017年。

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