MicroRNA-25表达下调对神经胶质瘤U87细胞增殖与凋亡的影响

目的探讨microRNA-25（miR-25）表达下调对神经胶质瘤U87 细胞增殖与凋亡的影响，以及miR-25 与B 细胞淋巴瘤/ 白血病-2 基因（Bcl-2）在胶质瘤细胞增殖与凋亡过程中的调节作用。方法通过慢病毒介导反义miR-25 寡聚核苷酸转染U87 细胞；分为3 组，实验组（转染anti-miR-25）、对照组（转染negative control）和空白组（空白PBS）；实时荧光定量聚合酶链反应（qRT-PCR）检测miR-25 和Bcl-2 的mRNA 表达水平；CCK-8 法检测细胞增殖情况；流式细胞术检测细胞周期和细胞凋亡。结果实验组miR-25 和Bcl-2 的mRNA 表达量与空白组和对照组比较，差异具有统计学意义（P <0.05），实验组降低；实验组相对于空白组和对照组，细胞增殖活性降低，细胞周期延缓，细胞凋亡率升高。结论在胶质瘤U87 细胞，miR-25 表达下调通过作用于Bcl-2 靶基因，延缓细胞周期，抑制细胞增殖，促进细胞凋亡。

Effect of down-regulation of miR-25 expression on proliferation and apoptosis of glioma U87 cells

Objective To study the effect of down-regulation of miR-25 expression on the proliferation and apop- tosis of glioma U87 cells, and the regulatory effect of miR-25 and its target gene Bcl-2 on the proliferation and apoptosis process of glioma cells. Methods U87 cells were transfected by lentiviral-mediated antisense miR-25 oligonucleotides. In the experiment groups (transfected with anti-miR-25), control groups (transfected with negative control) and blank groups (blank PBS), RT-PCR was used to detect the mRNA expression levels of miR-25 and Bcl-2, CCK method was used to detect cell proliferation, flow cytometry was used to detect the cell cycle and apop-tosis. Results The mRNA expression levels of miR-25 and Bcl-2 in the experiment groups were lower than those in the the blank groups and the control groups, the differences were statistically significant (p < 0.05). Compared with the blank groups and the control groups, the cell proliferation activity was decreased, the cell cycle was delayed and the apoptosis rate was increased in the experiment groups. Conclusions In glioma U87 cells, down-regulation of miR-25 expression delays cell cycle, inhibits cell proliferation, and promotes apoptosis by targeting Bcl-2 gene.