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Cannabidiol Induces Cell Cycle Arrest and Cell Apoptosis in Human Gastric Cancer SGC-7901 Cells

机译:大麻诱导人胃癌SGC-7901细胞中细胞周期滞留和细胞凋亡

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摘要

The main chemical component of cannabis, cannabidiol (CBD), has been shown to have antitumor properties. The present study examined the in vitro effects of CBD on human gastric cancer SGC-7901 cells. We found that CBD significantly inhibited the proliferation and colony formation of SGC-7901 cells. Further investigation showed that CBD significantly upregulated ataxia telangiectasia-mutated gene (ATM) and p53 protein expression and downregulated p21 protein expression in SGC-7901 cells, which subsequently inhibited the levels of CDK2 and cyclin E, thereby resulting in cell cycle arrest at the G0−G1 phase. In addition, CBD significantly increased Bax expression levels, decreased Bcl-2 expression levels and mitochondrial membrane potential, and then upregulated the levels of cleaved caspase-3 and cleaved caspase-9, thereby inducing apoptosis in SGC-7901 cells. Finally, we found that intracellular reactive oxygen species (ROS) increased after CBD treatment. These results indicated that CBD could induce G0−G1 phase cell cycle arrest and apoptosis by increasing ROS production, leading to the inhibition of SGC-7901 cell proliferation, thereby suggesting that CBD may have therapeutic effects on gastric cancer.
机译:已显示大麻,大麻组的主要化学成分,已显示具有抗肿瘤性质。本研究检测了CBD对人胃癌SGC-7901细胞的体外影响。我们发现CBD显着抑制了SGC-7901细胞的增殖和菌落形成。进一步的研究表明,CBD显着上调过度增长的Ataxia Telanciectasia-突变的基因(ATM)和P53蛋白表达,并在SGC-7901细胞中进行下调的P21蛋白表达,随后抑制CDK2和细胞周期蛋白E的水平,从而导致G0处的细胞周期捕获-g1阶段。此外,CBD显着增加了Bax表达水平,降低了Bcl-2表达水平和线粒体膜电位,然后上调了切割的胱天蛋白酶-3和切割的Caspase-9的水平,从而在SGC-7901细胞中诱导细胞凋亡。最后,我们发现CBD处理后细胞内反应性氧(ROS)增加。这些结果表明,CBD可以通过增加ROS生产来诱导G0-G1相细胞周期停滞和细胞凋亡,从而抑制SGC-7901细胞增殖,从而表明CBD可能对胃癌具有治疗作用。

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