miR-539对肺癌细胞增殖和凋亡作用的研究

目的 研究miR-539对非小细胞肺癌细胞增殖和凋亡的调控作用.方法 通过荧光定量PCR检测非小细胞肺癌细胞系(A549、NCI-H358、NCI-H1650、NCI-H1299、HCC827)和正常人支气管上皮细胞(16HBE)中miR-539表达的差异;通过转染miR-539-mimics在NCI-H358细胞中上调miR-539的表达,并通过MTT和TUNEL法检测miR-539对非小细胞肺癌细胞(NCI-H358)增殖和凋亡的影响.结果 与正常人支气管上皮细胞相比,非小细胞肺癌细胞中miR-539的表达显著降低(P<0.01);与空白对照组和阴性对照组相比,过表达miR-539能显著降低非小细胞肺癌NCI-H358细胞的增殖能力并增加其对地塞米松诱导凋亡的敏感性(P<0.01,P<0.05).结论 miR-539能够抑制非小细胞肺癌细胞增殖并促进其凋亡,可作为非小细胞肺癌基因治疗的靶点.

Effect of miR-539 on Proliferation and Apoptosis of Lung Cancer Cells

Objective To investigate regulation effect of microRNA-539 (miR-539) on proliferation and apopto-sis of non-small cell lung cancer (NSCLC) cells. Methods Expressions of miR-539 in NSCLC cell line (A549, NCI-H358, NCI-H1650, NCI-H1299 and HCC827) and normal human bronchial epithelial (NHBE) cells (16HBE) were detected by fluorescent quantitation polymerase chain reaction ( PCR) method. miR-539 expression was up-regulated by transfecting miR-539-mimics into NCI-H358 cells, and then effects of miR-539 on proliferation and apoptosis of NSCLC cells (NCI-H358) were detected by MTT assay and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) method. Results miR-539 expression in NSCLC cells was significantly decreased compared with that in NHBE cells (P<0. 01). Proliferation ability of NCI-H358 NSCLC cells was significantly decreased, and its sensitivity to apoptosis induced by Dexamethasone was increased in over-expressed miR-539 group compared with those in control and negative groups (P<0. 01, P<0. 05). Conclusion MiR-539 can inhibit the proliferation of NSCLC cells and promote its apoptosis, which can be used as a target for gene therapy of NSCLC.