摘要
目的探索miR-181a-5p的抑癌机制,探讨其是否可作为临床检测肺癌的标志物。方法采用CCK8法检测非小细胞肺癌(non-small cell lung cancer,NSCLC)细胞株A549细胞增殖情况;流式细胞术检测细胞凋亡;细胞划痕和Transwell实验检测miR-181a-5p对A549细胞运动的影响;利用双荧光报告基因实验和RT-PCR实验探讨miR-181a-5p与靶基因的相互作用。结果在非小细胞肺癌细胞株A549中过表达miR-181a-5p能明显抑制A549细胞株的增殖,促进细胞的早期凋亡(P<0.05)。细胞划痕和Transwell实验结果表明miR-181a-5p能明显抑制细胞的运动(P<0.05);miR-181a-5p可通过3'UTR靶向下调Kras基因的表达,且在NSCLC中Kras表达与miR-181a-5p表达有一定关系。结论 miR-181a-5p可显著抑制NSCLC A549细胞的生物进程,是潜在的治疗NSCLC的靶标。
Objective The aims of this study were to explore the biologic functions of miR-181a-5p in NSCLC and investigate whether it can be a marker for detecting NSCLC. Methods A549 cell growth and apoptosis after transfected miR-181a-5p were examined by CCK8 and flow cytometry,respectively,the movement of A549 cell were detected by Transwell assay and wound healing assay. Interaction of miR-181a-5p and its possible target genes were detected by dual luciferase reporter assay. Results MiR-181a-5p inhibited A549 cell proliferation,promoted cell apoptosis in vitro. Transwell assay and wound healing assay showed that miR-181-5p negatively regulated cell migration in vitro. MiR-181a-5p down-regulated Kras expression by directly targeting its 3'-UTR. Kras was inversely correlated with miR-181a-5p expression in NSCLC. Conclusion MiR-181a-5p might provide a potential treatment approach for NSCLC patients.
出处
《中国生化药物杂志》
CAS
北大核心
2014年第6期6-10,共5页
Chinese Journal of Biochemical Pharmaceutics
基金
2011年国家自然科学基金(81172217)
