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首页> 外文期刊>Journal of Cellular Physiology >Chrysin induces death of prostate cancer cells by inducing ROS and ER stress
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Chrysin induces death of prostate cancer cells by inducing ROS and ER stress

机译：白杨素诱发前列腺癌细胞的死亡诱导活性氧和ER应激

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摘要

Chrysin is a natural flavone found in numerous plant extracts, honey, and propolis that has multiple biological activities including anti-cancer effects. Understanding of biological mechanisms mediated in response to chrysin in cancerous cells may provide novel insight into chemotherapeutic approaches with reduced side effects in cancers. In the present study, we investigated functional roles of chrysin in progression of prostate cancer cells using DU145 and PC-3 cell lines. The results showed that chrysin induced apoptosis of cells evidenced by DNA fragmentation and increasing the population of both DU145 and PC-3 cells in the sub-G(1) phase of the cell cycle. In addition, chrysin reduced expression of proliferating cell nuclear antigen in the prostate cancer cell lines compared to untreated prostate cancer cells. Moreover, chrysin induced loss of mitochondria membrane potential (MMP), while increasing production of reactive oxygen species (ROS) and lipid peroxidation in a dose-dependent manner. Also, it induced endoplasmic reticulum (ER) stress through activation of unfolded protein response (UPR) proteins including PRKR-like ER kinase (PERK), eukaryotic translation initiation factor 2 (eIF2), and 78kDa glucose-regulated protein (GRP78) in DU145 and PC-3 cells. The chrysin-mediated intracellular signaling pathways suppressed phosphoinositide 3-kinase (PI3K) and the abundance of AKT, P70S6K, S6, and P90RSK proteins, but stimulated mitogen-activated protein kinases (MAPK) and activation of ERK1/2 and P38 proteins in the prostate cancer cells. Collectively, these results indicate that chrysin initiates cell death through induction of mitochondrial-mediated apoptosis and ER stress, and regulation of signaling pathways responsible for proliferation of prostate cancer cells.
机译：白杨素是一种天然黄酮中发现众多植物提取物,蜂蜜,蜂胶多种生物活性包括抗癌效果。白杨素机制介导的反应癌细胞可能提供新颖的见解化疗方法降低的一面在癌症的效果。白杨素功能角色的调查使用DU145前列腺癌细胞的发展和曲泽细胞系。白杨素诱导凋亡细胞的证明了这一点DNA碎片和增加人口DU145和sub-G曲泽细胞(1)阶段的细胞周期。增殖细胞核的表达式抗原在前列腺癌症细胞系而未经治疗的前列腺癌细胞。此外,白杨素诱导线粒体的损失膜电位(MMP),而增加生产活性氧(ROS)脂质过氧化作用剂量依赖性的方式。此外,它诱导内质网(ER)压力通过激活的蛋白质响应(UPR)蛋白质包括PRKR-like ER激酶(活跃),真核翻译起始因子2 (eIF2), 78 kda glucose-regulated在DU145和曲泽细胞蛋白(GRP78)。chrysin-mediated细胞内信号通路抑制磷酸肌醇3-kinase (PI3K)和丰富的一种蛋白激酶,P70S6K S6和P90RSK蛋白质,但刺激增殖作用激活蛋白激酶(MAPK)和ERK1/2和P38蛋白在前列腺癌细胞。总的来说,这些结果表明,白杨素提升者通过诱导细胞死亡mitochondrial-mediated细胞凋亡和ER应激,和调节信号通路的责任对前列腺癌细胞扩散。

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