微小RNA-382-5p靶向作用核因子蛋白90对乳腺癌细胞增殖和凋亡的影响

目的 观察微小RNA-382-5p （miR-382-5p）对乳腺癌细胞增殖和凋亡的影响，并探讨其作用机制。方法 采用荧光实时定量聚合酶链反应（qPCR）的方法检测miR-382-5p在9例乳腺癌患者癌组织和乳腺癌细胞株中的表达，细胞计数试剂盒（CCK-8）法和平板克隆实验分别检测过表达miR-382-5p后乳腺癌细胞活力和增殖能力，流式细胞仪检测细胞凋亡情况。qPCR和Western blot法检测过表达miR-382-5p的乳腺癌细胞中核因子蛋白90（NF90）的表达。采用荧光素酶活性实验验证miR-382-5p对靶基因的靶向作用。结果 miR-382-5p在乳腺癌组织和细胞中低表达（P<0.05），过表达miR-382-5p可抑制乳腺癌细胞的增殖能力，促进细胞的凋亡（P<0.01）。转染miR-382-5p模拟物组NF90基因的相对表达量较miR-NC组明显降低（P<0.01）。荧光素酶活性实验显示miR-382-5p与NF90基因3''非翻译区存在靶向关系（P<0.01）。结论 miR-382-5p对乳腺癌细胞的增殖具有抑制作用，对细胞的凋亡具有促进作用，其机制与靶向抑制NF90基因表达有关。

Effect of MicroRNA-382-5p on the Proliferation and Apoptosis of Breast Cancer Cells by Regulating the Expression of Nuclear Factor Protein 90

Objective To observe the effect of microRNA-382-5p (miR-382-5p) on the proliferation and apoptosis of breast cancer cells and to explore its mechanism. Methods The expression of miR-382-5p in 9 cases of breast cancer tissues and breast cancer cell lines was detected by real-time quantitative polymerase chain reaction (qPCR). The cell counting kit (CCK-8) and plate cloning were used to detect the viability and proliferation of breast cancer cells after miR-382-5p was over-expressed. Apoptosis was detected by flow cytometry. The expression of NF90 in breast cancer cells was detected by qPCR and Western blot after miR-382-5p was over-expressed. The targeting effect of miR-382-5p on target gene NF90 was verified by luciferase activity assay. Results The expression of miR-382-5p was lower in breast cancer tissues and cells (P<0.05). Overexpression of miR-382-5p could inhibit the proliferation of breast cancer cells and promote cell apoptosis (P<0.01). The relative expression of NF90 gene in miR-382-5p group was significantly lower than that in miR-NC group(P<0.01). The luciferase activity assay showed that miR-382-5p had a targeted relationship with the 3''untranslated region of NF90 gene(P<0.01). Conclusion miR-382-5p can inhibit the proliferation of breast cancer cells and promote the apoptosis of breast cancer cells. The mechanism is related to the inhibition of NF90 gene expression.