菊花对pc-3人前列腺癌细胞的抗肿瘤作用是通过诱导凋亡、caspase信号通路和线粒体膜电位丧失介导的。

De-Kang Sun, Lin Wang, Peng Zhang
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引用次数: 11

摘要

背景:本研究的主要目的是研究菊花对人前列腺癌PC-3细胞的抗肿瘤和凋亡作用。材料与方法:采用MTT法观察菊花对细胞活力的影响,采用流式细胞术和荧光显微镜观察菊花对细胞凋亡的诱导作用。western blot检测对caspase活性的影响。结果:菊花对PC-3癌细胞的抑制作用呈时间依赖性和浓度依赖性。在10、50和150µM剂量下,菊花素处理的细胞凋亡率分别为34.2%、56.7%和69.1%。线粒体去极化的细胞比例从未处理细胞的5.3%增加到10、50和150µM剂量的细胞的27.2%、57.6%和86.9%。菊花还以剂量依赖性的方式增强了所有三种半胱天冬酶的活性,即半胱天冬酶-3、8和9。结论:本研究认为,菊花对PC-3前列腺癌细胞的抗癌作用可能是通过诱导细胞凋亡、激活caspas3信号通路、丧失线粒体膜电位等途径实现的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

ANTITUMOR EFFECTS OF CHRYSANTHEMIN IN PC-3 HUMAN PROSTATE CANCER CELLS ARE MEDIATED VIA APOPTOSIS INDUCTION, CASPASE SIGNALLING PATHWAY AND LOSS OF MITOCHONDRIAL MEMBRANE POTENTIAL.

ANTITUMOR EFFECTS OF CHRYSANTHEMIN IN PC-3 HUMAN PROSTATE CANCER CELLS ARE MEDIATED VIA APOPTOSIS INDUCTION, CASPASE SIGNALLING PATHWAY AND LOSS OF MITOCHONDRIAL MEMBRANE POTENTIAL.

ANTITUMOR EFFECTS OF CHRYSANTHEMIN IN PC-3 HUMAN PROSTATE CANCER CELLS ARE MEDIATED VIA APOPTOSIS INDUCTION, CASPASE SIGNALLING PATHWAY AND LOSS OF MITOCHONDRIAL MEMBRANE POTENTIAL.

ANTITUMOR EFFECTS OF CHRYSANTHEMIN IN PC-3 HUMAN PROSTATE CANCER CELLS ARE MEDIATED VIA APOPTOSIS INDUCTION, CASPASE SIGNALLING PATHWAY AND LOSS OF MITOCHONDRIAL MEMBRANE POTENTIAL.

Background: The main objective of the current research work was to investigate the antitumor and apoptotic effects of chrysanthemin in PC-3 human prostate cancer cells.

Materials and methods: MTT assay was used to evaluate the effects of chrysanthemin on cell viability whereas flow cytometry along with fluorescence microscopy were used to study apoptotic induction in these cells. Effects on caspase activation were detected through western blot assay.

Results: Results showed that chrysanthemin inhibited cancer cell growth in PC-3 cancer cells in a time-dependent as well as concentration-dependent manner. Chrysanthemin-treated cells at 10, 50 and 150 µM doses led to 34.2%, 56.7% and 69.1% apoptosis in these cells respectively. The percentage of cells with depolarized mitochondria increased from 5.3% in untreated control cells to 27.2%, 57.6% and 86.9% in cells treated with 10, 50 and 150 µM dose of chrysanthemin respectively. Chrysanthemin also enhanced the activity of all three caspases viz., caspase-3, 8 and 9 in a dose-dependent fashion.

Conclusions: The study concluded that chrysanthemin ledanticancer effects in PC-3 prostate cancer cells by inducing apoptosis, activating caspasesignaling pathway and loss of mitochondrial membrane potential.

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