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Evodiamine Inhibits the Proliferation of BGC-823 and SGC-7901 Cells by Inducing Cell Cycle Arrest and Apoptosis in Gastric Cancer

机译:Evodiamine通过诱导胃癌细胞周期阻滞和凋亡抑制BGC-823和SGC-7901细胞的增殖

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Gastric cancer represents a major cause of cancer-related death worldwide. Although various tactics and anti-tumor drugs have been used to improve curative effects, five-year survival rate of lung cancer patients remains poor. Evodiamine, a sophora alkaloid, has been demonstrated to exert antitumor effects on many types of cancer. However, the molecular mechanism of evodiamine against gastric cancer has not been clearly elucidated. In this study, we investigated the anti-tumor activity and the underlying mechanisms of EVO on gastric cancer cells, and found that it significantly inhibited the proliferation of BGC-823 and SGC-7901 cells by inducing cell cycle arrest at G2/M phase and cell apoptosis in a dose- and time-dependent manner. Its molecular mechanism may be that it reduces the expression of cell cycle- promoting protein Cdc25C and promotes the expression of cell cycle inhibitor p53, as well as prompts the activity of caspases pathways, such as the expression level of cleaved caspase-3 and cleaved caspase-8; cleaved caspase-9 and cleaved PARP-1 are up-regulated, treated with EVO (10 μM) at different points in time (0, 3, 6, 9, 12, 24 h). Collectively, our data demonstrated that EVO was a potential anti-tumor agent against gastric cancer.
机译:胃癌是全世界癌症相关死亡的主要原因。尽管已经使用各种策略和抗肿瘤药物来改善疗效,但是肺癌患者的五年生存率仍然很差。 Evodiamine是一种槐花生物碱,已被证明可对多种类型的癌症发挥抗肿瘤作用。但是,尚不清楚阐明依维他命抗胃癌的分子机制。在这项研究中,我们研究了EVO对胃癌细胞的抗肿瘤活性及其潜在机制,并发现EVO通过诱导G2 / M期细胞周期停滞并显着抑制BGC-823和SGC-7901细胞的增殖。细胞凋亡呈剂量和时间依赖性。其分子机制可能是它降低了细胞周期促进蛋白Cdc25C的表达,并促进了细胞周期抑制剂p53的表达,并促进了胱天蛋白酶途径的活性,如裂解的caspase-3和裂解的caspase的表达水平。 -8;裂解的caspase-9和裂解的PARP-1被上调,在不同时间点(0、3、6、9、12、24 h)用EVO(10μM)处理。总体而言,我们的数据表明EVO是潜在的抗胃癌抗肿瘤药。

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