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Cantharidin induces G2/M phase arrest and apoptosis in human gastric cancer SGC-7901 and BGC-823 cells

机译:斑th素诱导人胃癌SGC-7901和BGC-823细胞G2 / M期阻滞和凋亡

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摘要

The aim of the present study was to investigate the effect of cantharidin (CTD) on human gastric cancer cells and to explore the underlying mechanisms of these effects. The human gastric cancer SGC-7901 and BGC-823 cell lines were treated with CTD. MTS assays were then employed to examine cellular proliferation, flow cytometry was used to analyze the cell cycle and apoptosis, and western blot analysis was used to determine protein expression levels. It was found that CTD inhibited the proliferation of the human gastric cancer SGC-7901 and BGC-823 cells in a dose- and time-dependent manner in vitro. CTD also induced G2/M phase arrest and cellular apoptosis in a dose-dependent manner. In addition, CTD increased the levels of p21, caspase-7, -8 and -9, activated caspase-3, poly ADP ribose polymerase and Bad, but decreased the levels of cyclin-dependent kinase 1, cyclin A and B, B-cell lymphoma-2 (Bcl-2) and Bid. The present results suggested that CTD may inhibit the proliferation of human gastric cancer SGC-7901 and BGC-823 cells in vitro by inducing G2/M phase arrest and cell apoptosis. CTD may induce cellular G2/M phase arrest by regulating cycle-associated proteins and induce apoptosis by activating a caspase cascade or regulating the Bcl-2 family proteins.
机译:本研究的目的是研究cantharidin(CTD)对人胃癌细胞的作用,并探讨这些作用的潜在机制。用CTD处理人胃癌SGC-7901和BGC-823细胞系。然后使用MTS分析检查细胞增殖,使用流式细胞仪分析细胞周期和细胞凋亡,并使用Western blot分析确定蛋白表达水平。发现CTD在体外以剂量和时间依赖性方式抑制人胃癌SGC-7901和BGC-823细胞的增殖。 CTD还以剂量依赖性方式诱导G2 / M期阻滞和细胞凋亡。此外,CTD增加了p21,caspase-7,-8和-9,活化的caspase-3,聚ADP核糖聚合酶和Bad的水平,但降低了细胞周期蛋白依赖性激酶1,cyclin A和B,B-的水平细胞淋巴瘤2(Bcl-2)和出价。目前的结果表明,CTD可能通过诱导G2 / M期阻滞和细胞凋亡来抑制人胃癌SGC-7901和BGC-823细胞的体外增殖。 CTD可能通过调节周期相关蛋白诱导细胞G2 / M期阻滞,并通过激活半胱天冬酶级联反应或调节Bcl-2家族蛋白诱导细胞凋亡。

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