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首页> 外文期刊>Molecular medicine reports >Ailanthone induces G(2)/M cell cycle arrest and apoptosis of SGC-7901 human gastric cancer cells
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Ailanthone induces G(2)/M cell cycle arrest and apoptosis of SGC-7901 human gastric cancer cells

机译：果莲酮诱导G（2）/ m细胞周期骤停和SGC-7901人胃癌细胞的凋亡

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摘要

Ailanthone is a major quassinoid extracted from the Chinese medicinal herb Ailanthus altissima, which has been reported to exert antiproliferative effects on various cancer cells. The present study aimed to investigate the antitumor effects of ailanthone on SGC-7901 cells, and to analyze its underlying molecular mechanisms. Following treatment with ailanthone, Cell Counting kit-8 was used to detect the cytotoxic effects of ailanthone on SGC-7901 cells in vitro. The typical apoptotic morphology of SGC-7901 cells was observed by Hoechst 33258 staining. Cell cycle progression and apoptosis were measured by flow cytometry, and the protein and mRNA expression levels of Bcl-2 and Bax were analyzed by western blot analysis and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) respectively, in SGC-7901 cells. The results of the present study indicated that ailanthone inhibited the proliferation of SGC-7901 cells in a dose- and time-dependent manner in vitro, and also demonstrated that ailanthone induced G2/M phase cell cycle arrest and apoptosis of SGC-7901 cells. Furthermore, analysis of the underlying molecular mechanisms revealed that ailanthone downregulated the expression levels of Bcl-2, whereas the expression levels of Bax were upregulated at the protein and mRNA levels. In conclusion, ailanthone may inhibit the proliferation of SGC-7901 cells by inducing G2/M phase cell cycle arrest and apoptosis via altering the protein and mRNA expression levels of Bcl-2 and Bax in SGC-7901 cells.
机译：艾西兰酮是从中药草药Altissima中提取的主要杂星，据报道，据报道，对各种癌细胞产生抗增殖作用。本研究旨在探讨胃仙酮对SGC-7901细胞的抗肿瘤作用，并分析其潜在的分子机制。在用硫酮处理后，使用细胞计数试剂盒-8来检测在体外SGC-7901细胞对均蒽的细胞毒性作用。通过Hoechst 33258染色观察SGC-7901细胞的典型凋亡形态。通过流式细胞术测量细胞周期进展和细胞凋亡，通过蛋白质印迹分析和逆转录定量聚合酶链反应（RT-QPCR）分析Bcl-2和Bax的蛋白质和mRNA表达水平，在SGC-7901细胞中分析。本研究的结果表明，硫代以体外剂量和时间依赖性方式抑制SGC-7901细胞的增殖，并表明硫酮诱导了SGC-7901细胞的G2 / M期细胞周期停滞和凋亡。此外，潜在的分子机制的分析表明，吡喃酮下调了Bcl-2的表达水平，而在蛋白质和mRNA水平上上调败血症的表达水平。总之，通过在SGC-2和SGC-7901细胞中改变Bcl-2和Bax的蛋白质和mRNA表达水平，通过诱导G2 / M相细胞周期停滞和凋亡，嗜硅酮可以抑制SGC-7901细胞的增殖。

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