| 二甲双胍联合阿帕替尼对胃癌细胞的增殖抑制作用 |
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| 引用本文： | 穆春青,吴梦瑶,李红.二甲双胍联合阿帕替尼对胃癌细胞的增殖抑制作用[J].现代预防医学,2019,0(14):2671-2675. |
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| 作者姓名： | 穆春青 吴梦瑶 李红 |
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| 作者单位： | 锦州医科大学生化教研室，辽宁 锦州 121000 |
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| 摘 要： | 目的 探讨二甲双胍联合阿帕替尼对胃癌BGC823细胞系的增殖抑制作用及其可能的机制。方法 MTT法检测不同浓度二甲双胍（0～30 mmol/L)、不同浓度阿帕替尼（0～60 μmol/L）及两药联合应用处理BGC823细胞24、48、72 h的增殖抑制率，结晶紫染色法检测细胞集落形成能力，流式细胞术检测细胞凋亡，western blot检测细胞中血管内皮生长因子信号通路及凋亡相关蛋白VEGFR2、PI3K、p - AKT、AKT、Bax、Bcl - 2表达水平。结果 二甲双胍和阿帕替尼单独处理BGC823后，细胞增殖抑制率均增加（P＜0.05），联合用药产生协同作用（CI＜1），二甲双胍和阿帕替尼单独及联合应用均能抑制细胞集落形成并使总凋亡比例增加（P＜0.05）。与对照组和单药组相比，联合用药可明显下调细胞中VEGFR2、PI3K、p - AKT、AKT、Bcl - 2蛋白的表达水平，上调Bax蛋白表达水平（P＜0.05）。结论 二甲双胍联合阿帕替尼具有协同抑制胃癌BGC823细胞增殖和诱导细胞凋亡的作用，其机制可能与抑制VEGF信号通路有关。
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| 关 键 词： | 二甲双胍 胃癌 VEGF信号通路 增殖 阿帕替尼 |
Inhibitory effect of metformin combined with apatinib on proliferation of gastric cancer cells |
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| MU Chun-qing,WU Meng-yao,LI Hong.Inhibitory effect of metformin combined with apatinib on proliferation of gastric cancer cells[J].Modern Preventive Medicine,2019,0(14):2671-2675. |
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| Authors: | MU Chun-qing WU Meng-yao LI Hong |
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| Affiliation: | Department of Biochemistry, Jinzhou Medical University, Jinzhou, Liaoning 121000, China |
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| Abstract: | Objective To investigate the possible mechanism of the inhibitory effect of metformin combined with apatinib on the proliferation of BGC823 cell line. Methods The gastric cancer BGC823 cells were treated with 0-30 mmol/L metformin, 0-60 μmol/L apatinib, and the combination of the two drugs for 24 h, 48 h and 72 h, The cell proliferation inhibition rate was detected by MTT assay, and the colony formation ability was detected by crystal violet staining, apoptosis by flow cytometry, vascular endothelial growth factor signaling pathway and apoptosis related proteins VEGFR2, PI3K, p-AKT, AKT, Bax and Bcl-2 by Western blot. Results The cell proliferation inhibition rate of gastric cancer BGC823 cell line increased after being treated by metformin, or apatinib alone (P<0.05). metformin combined with apatinib had a synergistic effect (CI<1). Metformin and apatinib taken alone or in combination inhibited the formation of cell colonies, and the proportion of total apoptosis increased(P<0.05). Compared with the control group and the experimental group treated by single drug, the expression levels of VEGFR2, PI3K, p-AKT, AKT and Bcl-2 proteins were significantly decreased, and the expression level of Bax protein was increased in the group treated with combinations of drugs(P<0.05). Conclusion Metformin combined with apatinib had a synergistic effect on BGC823 cell line and this combined therapy induced cell apoptosis, which may be related to the inhibition of VEGF signaling pathway. |
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| Keywords: | Metformin Gastric cancer VEGF signaling pathway Proliferation Apatinib |
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