华蟾素对非小细胞肺癌细胞株A549细胞增殖及PTEN/AKT/mTOR信号通路表达的影响 |
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引用本文: | 张生义,张己为,张旭峰,张逸,许斌斌,左顺庆. 华蟾素对非小细胞肺癌细胞株A549细胞增殖及PTEN/AKT/mTOR信号通路表达的影响[J]. 蚌埠医学院学报, 2020, 45(9): 1159-1162. DOI: 10.13898/j.cnki.issn.1000-2200.2020.09.004 |
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作者姓名: | 张生义 张己为 张旭峰 张逸 许斌斌 左顺庆 |
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作者单位: | 上海市松江区中心医院 胸外科, 201600 |
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摘 要: | 目的观察华蟾素对肺癌细胞A549及PTEN/AKT/mTOR信号通路蛋白表达的影响。方法在培养肺癌细胞株NCI-A549中分别加入不同浓度的华蟾素,应用细胞计数试剂盒-8检测24、48、72 h后细胞增殖活力,Ki67及EdU检测72 h细胞增殖活力,免疫印迹法检测磷脂酰肌醇-3激酶/蛋白激酶B/哺乳动物雷帕霉素靶蛋白以及磷酸化第10号染色体缺失的磷酸酶和张力蛋白的同源基因(phosphorylated-phosphatase and tensin homolog deleted on chromosome ten,p-PTEN)蛋白表达。结果0.2 μg/mL华蟾素作用于A549细胞株48 h后显示明显抑制增殖作用(P < 0.01),0.8 μg/mL华蟾素处理12 h后均具有不同程度抑制增殖作用(P < 0.05~P < 0.01)。不同浓度华蟾素作用于细胞72 h后,p-PI3K、p-AKT、p-mTOR、p-S6、p-PTEN表达量均较对照组下降(P < 0.05~P < 0.01),而PI3K、AKT、mTOR、S6及PTEN表达量与对照组差异无统计学意义(P>0.05)。结论华蟾素可能通过抑制PI3K/AKT/mTOR信号通路蛋白磷酸化,抑制肺癌细胞A549的增殖。
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关 键 词: | 肺肿瘤 华蟾素 肺癌细胞株A549 PTEN/AKT/mTOR信号通路 增殖 |
收稿时间: | 2019-11-20 |
Effect of cinobufacin on the proliferation and expression of PTEN/AKT/mTOR signaling pathway in non-small cell lung cancer cell line A549 |
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Affiliation: | Department of Thoracic Surgery, Songjiang Central Hospital of Shanghai, Shanghai 201600, China |
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Abstract: | ObjectiveTo observe the expression changes of PTEN/AKT/mTOR signaling pathway protein after the lung cancer cells A549 treated with cinobufacin.MethodsDifferent concentrations of cinobufacin were added to the cultured lung cancer cell line NCI-A549, and the cell proliferation activity was measured using cell counting kit-8 after 24, 48 and 72 h.Ki67 and EdU were used to detect the proliferation of cells after 72 h of treatment with cinobufacin.Western blotting was used to detect the expression levels of protein kinase B/mammalian rapamycin target protein pathway protein(AKT/mTOR) and phosphorylated-phosphatase and tensin homolog deleted on chromosome ten(P-PTEN).ResultsThe proliferation of A549 cell line inhibited after treatment with 0.2 μg/mL cinobufacin for 48 h(P < 0.01), and the proliferation of A549 cell line was inhibited after treatment with 0.8 μg/mL cinobufacin for 12 h(P < 0.05 to P < 0.01).Compared with the control group, the expression levels of p-PI3K, p-AKT, p-mTOR, p-S6 and p-PTEN in experimential group after 72 h of treatment with different concentrations of cinobufacin decreased(P < 0.05 to P < 0.01), while the differences of the expression levels of PI3K, AKT, mTOR, S6 and PTEN were not statistically significant between the control group and erperimantial group(P>0.05).ConclusionsCinobufacin may inhibit the proliferation of lung cancer cells A549 by inhibiting the phosphorylation of PI3K/AKT/mTOR signaling pathway protein. |
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