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目的研究5‐氮‐2‐脱氧胞苷(5‐aza‐2‐deoxycytidine ,5‐Aza)对胃癌细胞株GC‐7901自噬、凋亡及胰岛素相关信号通路轴的影响。方法选择不同浓度(5μmol/L、10μmol/L、20μmol/L )的5‐Aza干预胃癌细胞株GC‐7901,72 h后用免疫印记检测自噬相关蛋白LC3‐Ⅱ和LC3‐Ⅰ的表达。选择5‐Aza最佳浓度10μmol/L干预GC‐7901,免疫印记检测空白组和对照组中胰岛素样生长因子‐1受体(IGF‐1R)、磷酸化胰岛素样生长因子‐1受体(p‐IGF‐1R)及下游信号通路相关蛋白磷脂酰肌醇3‐激酶(PI3K )、哺乳动物雷帕霉素靶蛋白(mTOR),磷酸化磷脂酰肌醇3‐激酶(p‐PI3K)、磷酸化哺乳动物雷帕霉素靶蛋白(p‐mTOR)的表达;流式细胞技术检测细胞凋亡情况。结果不同浓度的5‐Aza均可增加胃癌细胞的自噬表达,并呈计量依赖性,10μmol/L 5‐Aza干预后胃癌细胞的状态最佳。10μmol/L 5‐Aza可诱导胃癌细胞株GC‐7901凋亡增加,5‐Aza组与空白对照组相比较差异具有显著性( P <0.01);10μmol/L 5‐Aza可抑制p‐IGF‐1R、p‐PI3K、p‐mTOR的表达,空白组与5‐Aza组相比较差异具有显著性( P <0.01)。但对总蛋白IGF‐1R、PI3K、mTOR无影响( P>0.05)。结论5‐Aza可以诱导胃癌细胞凋亡,增加细胞自噬,可能与抑制IGF‐1R磷酸化表达有关。“,”[Objective]To explore the effects of 5‐Aza‐2‐deoxycytidine (5‐Aza) on apoptosis ,autophagy and in‐sulin signal pathway in GC‐7901 cell line .[Methods]GC‐7901 cells were treated with 5 ,10 and 20μmol/L of 5‐Aza for 3 days .The expressions of autophagy‐related proteins LC3‐Ⅱ and LC3‐Ⅰwere detected by Western blot .And 10μmol/L5‐Aza was used for intervening GC‐7901 .Two groups of control and 5‐Aza were assigned .The expressions of insulin signaling axis associated proteins IGF‐1R and p‐IGF‐1R were detected by Western blot .And the expressions of IGF‐1R downstream signaling pathway related proteins PI3K ,p‐PI3K ,mTOR ,p‐mTOR were measured .Annexin V‐PI flow cytometry was used for detecting apoptotic cells .[Results]5‐Aza dose‐dependently decreased the level of LC3‐Ⅰand increased the level of LC3‐Ⅱ .And a significant increase in LC3‐Ⅱ/LC3‐Ⅰratio suggested that demethylating agent could significantly increase autophagy in gastric cancer cells .Cell autophagy and apoptosis could be induced by 5‐Aza .The expressions of phosphorylated insulin signaling pathway related proteins ,such as p‐IGF‐1R ,p‐PI3K and p‐mTOR ,significantly decreased .But it had no effect on total protein IGF‐1R ,PI3K or mTOR .[Conclusion]5‐Aza can induce cell autophagy and apoptosis and decrease the levels of phospho‐IGF‐1R , phospho‐PI3K and phospho‐mTOR proteins .However ,there is no effect on the total protein levels .