Lipocalin-2过表达对人肺癌 A549细胞增殖、凋亡及侵袭力的影响

目的：采用基因过表达方法上调人肺癌 A549细胞 Lipocalin-2表达，观察 Lipocalin-2对细胞增殖、凋亡、细胞周期调控及侵袭力的影响。方法构建 Lipocalin-2过表达慢病毒载体，转染人肺癌 A549细胞。Real-time PCR 和 Western blot 检测转染后人肺癌 A549细胞中 Lipocalin-2表达水平。MTT 实验检测细胞增殖。流式细胞术检测细胞周期及凋亡情况。Transwell 小室实验检测细胞侵袭力。结果与阴性对照组和空载体对照组比较，转染组 Li-pocalin-2 mRNA 和蛋白表达水平均显著增加，差异有统计学意义（ P ﹤0.05）。Lipocalin-2过表达慢病毒载体转染后，细胞增殖率和侵袭力显著增加，同时细胞凋亡率及 G0/ G1期细胞比例显著降低，S 期细胞比例显著提高，差异有统计学意义（ P ﹤0.05）。结论 Lipocalin-2过表达通过调控人肺癌 A549细胞周期、抑制凋亡促进细胞的增殖，还明显提高细胞的侵袭力。

Effects of overexpression of Lipocalin-2 on proliferation,apoptosis and invasiveness in human lung cancer A549 cells in vitro

Objective To investigate the effects of overexpression of Lipocalin-2 on cell proliferation,cell apoptosis, cell cycle regulation and invasiveness in human lung cancer A549 cells in vitro through up - regulating the expression levels of Lipocalin-2. Methods Lipocalin-2 gene coding region was cloned into lentivirus vector,then lentivirus particles were transfected into A549 cells to up-regulate the expression levels of Lipocalin-2 gene. The expression levels of Lipocalin-2 mRNA and protein were detected by Real-time PCR and Western Blot,respectively. The cell proliferation was determined by MTT assay and cell apoptosis and cell cycle were detected by flow cytometry. The cell invasiveness was measured by Transwell test. Results The expression levels of Lipocalin-2 mRNA and protein were increased significantly after the transfection,as compared with those in negative control group or empty vector control group( P ﹤ 0. 05). Moreover the cell proliferation rate and invasiveness were significantly increased,however,the cell apoptosis rate and ratio of G0 / G1 were obviously decreased, but the cell proportion at stage S was significantly increased( P ﹤ 0. 05). Conclusion The overexpression of Lipocalin-2 can promote proliferation of A549 cells through regulating cell cycle and inhibiting cell apoptosis.