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首页> 外文期刊>Asian Pacific Journal of Cancer Prevention >Roles of p53 and Caspases in Induction of Apoptosis in MCF-7 Breast Cancer Cells Treated with a Methanolic Extract of Nigella Sativa Seeds
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Roles of p53 and Caspases in Induction of Apoptosis in MCF-7 Breast Cancer Cells Treated with a Methanolic Extract of Nigella Sativa Seeds

机译:黑麦草种子甲​​醇提取物处理p53和胱天蛋白酶在诱导MCF-7乳腺癌细胞凋亡中的作用

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Background: Nigella Sativa (NS) is an herb from the Ranunculaceae family that exhibits numerous medicinalproperties and has been used as important constituent of many complementary and alternative medicines (CAMs).The ability of NS to kill cancer cells such as PC3, HeLa and hepatoma cells is well established. However, ourunderstanding of the mode of death caused by NS remains nebulous. The objective of this study was to gainfurther insight into the mode and mechanism of death caused by NS in breast cancer MCF-7 cells. Materialsand Methods: Human breast cancer cells (MCF-7) were treated with a methanolic extract of NS, and a dose- andtime-dependent study was performed. The IC50 was calculated using a Cell Titer Blue? viability assay assay, andevidence for DNA fragmentation was obtained by fluorescence microscopy TUNEL assay. Gene expression wasalso profiled for a number of apoptosis-related genes (Caspase-3, -8, -9 and p53 genes) through qPCR. Results:The IC50 of MCF-7 cells was 62.8μL/mL. When MCF-7 cells were exposed to 50 μL/mL and 100 μL/mL NS for24h, 48h and 72h, microscopic examination (TUNEL assay) revealed a dose- and time-dependent increase inapoptosis. Similarly, the expression of the Caspase-3, -8, -9 and p53 genes increased significantly according to thedose and time. Conclusions: NS induced apoptosis in MCF-7 cells through both the p53 and caspase pathways.NS could potentially represent an alternative source of medicine for breast cancer therapy.
机译:背景:Nigella Sativa(NS)是毛the科的一种草药,具有许多药用特性,已被用作许多辅助和替代药物(CAMs)的重要成分.NS杀死PC3,HeLa和肝癌等癌细胞的能力细胞已经建立。但是,我们对由NS引起的死亡方式的理解仍然不清楚。这项研究的目的是进一步了解乳腺癌MCF-7细胞中由NS引起的死亡的模式和机制。材料和方法:用NS的甲醇提取物处理人乳腺癌细胞(MCF-7),并进行剂量和时间依赖性研究。使用Cell Titer Blue?计算IC50。通过荧光显微镜TUNEL分析获得了活力分析,并获得了DNA片段化的证据。还通过qPCR分析了许多凋亡相关基因(Caspase-3,-8,-9和p53基因)的基因表达。结果:MCF-7细胞的IC50为62.8μL/ mL。当将MCF-7细胞分别暴露于50μL/ mL和100μL/ mL NS中24h,48h和72h时,显微镜检查(TUNEL分析)显示出细胞凋亡的剂量和时间依赖性增加。同样,Caspase-3,-8,-9和p53基因的表达随剂量和时间而显着增加。结论:NS通过p53和caspase途径诱导MCF-7细胞凋亡,NS可能代表了乳腺癌治疗的另一种药物来源。

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