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目的:探讨基于RNA干扰CMTM7对肺腺癌A549细胞凋亡的影响。方法:选择肺腺癌A549细胞株分为si RNA组、阴性对照组与空白对照组,在对数生长的A549细胞中转染RNA干扰CMTM7载体、脂质体空载体和不进行转染,观察A549细胞的生长、凋亡与细胞周期状况。结果:MTT实验显示si RNA转染组的抑制率明显高于阴性对照组和空白对照组(P<0.05),阴性对照组与空白对照组的对比无明显差异(P>0.05)。流式细胞术实验表明si RNA转染组的细胞凋亡率明显高于阴性对照组和空白对照组(P<0.05),阴性对照组与空白对照组的对比无明显差异(P>0.05)。流式细胞术实验表明si RNA转染组的G0/G1期细胞数目较阴性对照组和空白对照组增多明显(P<0.05),同时si RNA转染组的S、G2/M期细胞数目较阴性对照组和空白对照组明显减少(P<0.05),阴性对照组和空白对照组对比差异无统计学意义(P>0.05)。结论:RNA干扰CMTM7能够促进肺腺癌A549细胞凋亡,抑制肿瘤细胞的生长,其作用机制可能通过干扰细胞周期而实现。
Objective: To investigate the effect of CMTM7 RNA interference on the apoptosis of lung adenocarcinoma A549 cells. Methods: The lung adenocarcinoma A549 cell line was selected and divided into si RNA group, negative control group and blank control group. A549 cells were transfected with RNA interference CMTM7 vector, empty vector and transfected without transfection A549 cell growth, apoptosis and cell cycle status. Results: The inhibition rate of si RNA transfection group was significantly higher than that of negative control group and blank control group by MTT assay (P <0.05). There was no significant difference between negative control group and blank control group (P> 0.05). Flow cytometry showed that the rate of apoptosis in si RNA transfected group was significantly higher than that in negative control group and blank control group (P <0.05). There was no significant difference between negative control group and blank control group (P> 0.05). The results of flow cytometry showed that the number of cells in G0 / G1 phase of si RNA transfection group increased significantly compared with that of negative control group and blank control group (P <0.05). Meanwhile, the number of cells in S, G2 / M phase in si RNA transfected group was significantly Negative control group and blank control group were significantly reduced (P <0.05), negative control group and blank control group, the difference was not statistically significant (P> 0.05). Conclusion: RNA interference CMTM7 can promote the apoptosis of lung adenocarcinoma A549 cells and inhibit the growth of tumor cells. Its mechanism may be through interfering with the cell cycle.