抑制lncRNA LINC01503通过靶向调控miR-335-5p对肺癌细胞活力、迁移和侵袭的影响及其机制研究

目的:探讨长链非编码RNA(lncRNA)LINC01503对肺癌细胞活力、迁移和侵袭的影响及其作用机制。方法:将人肺癌H1299细胞分为si-NC组(转染si-NC)、si-LINC01503组(转染si-LINC01503)、pcDNA组(转染pcDNA)、pcDNA-LINC01503组(转染pcDNA-LINC01503)、miR-NC组(转染miR-NC)、miR-335-5p组(转染miR-335-5p mimics)、si-LINC01503+anti-miR-NC组(共转染si-LINC01503和anti-miR-NC)、si-LINC01503+anti-miR-335-5p组(共转染si-LINC01503和anti-miR-335-5p)、miR-NC+WT-LINC01503组(共转染miR-NC和WT-LINC01503)、miR-NC+MUT-LINC01503组(共转染miR-NC和MUT-LINC01503)、miR-335-5p+WT-LINC01503组(共转染miR-335-5p和WT-LINC01503)和miR-335-5p+MUT-LINC...

Effect of inhibiting lncRNA LINC01503 on viability,migration and invasion of lung cancer cells by targeted regulation of miR-335-5p

AIM:To investigate the effects of long non-coding RNA(lncRNA)LINC01503 on the viability,migration and invasion of lung cancer cells and its mechanism.METHODS:Human lung carcinoma H1299 cells were divided into si-NC group(transfected with si-NC),si-LINC01503 group(transfected with si-LINC01503),pcDNA group(transfected with pcDNA),pcDNA-LINC01503 group(transfected with pcDNA-LINC01503),miR-NC group(transfected with miR-NC),miR-335-5p group(transfected with miR-335-5p mimics),si-LINC01503+anti-miR-NC group(cotransfected with si-LINC01503 and anti-miR-NC),si-LINC01503+anti-miR-335-5p group(co-transfected with siLINC01503 and anti-miR-335-5p),miR-NC+WT-LINC01503 group(co-transfected with miR-NC and WT-LINC01503),miR-NC+MUT-LINC01503 group(co-transfected with miR-NC and MUT-LINC01503),miR-335-5p+WT-LINC01503 group(co-transfected with miR-335-5p and WT-LINC01503)and miR-335-5p+MUT-LINC01503 group(co-transfected with miR-335-5p and MUT-LINC01503).The expression of miR-335-5p and LINC01503 was detected by RT-qPCR.Western blot was used to detect protein expression.MTT assay was used to detect cell viability.Transwell assay was used to detect the migration and invasion abilities.Dual-luciferase reporter assay was used to confirm the targeted relationship between LINC01503 and miR-335-5p.RESULTS:Compared with normal tissues,the expression of LINC01503 was significantly increased in the lung cancer tissues,and the expression of miR-335-5p was significantly decreased(P<0.05).Compared with stage I/II,the expression level of LINC01503 in the lung cancer tissues of stage III/IV was significantly increased,and the expression of miR-335-5p was significantly decreased(P<0.05).The patients with high expression of LINC01503 had lower short-term survival rates than those with low expression of LINC01503(P<0.05).Compared with normal human bronchial epithelial cell line BEAS-2 B,the expression of miR-335-5p in lung cancer cell lines H1299,A549 and SPC-A-1 were significantly decreased,and the expression of LINC01503 was significantly increased(P<0.05).Over-expression of miR-335-5p and inhibition of LINC01503 expression inhibited the viability,migration and invasion of H1299 cells,and inhibited the protein expression of cyclin D1,matrix metalloproteinase-2(MMP-2)and MMP-9(P<0.05).LINC01503 targeted and regulated miR-335-5p expression,and interfering with miR-335-5p expression reversed the inhibitory effect of inhibiting LINC01503 expression on the viability,migration and invasion of H1299 cells.CONCLUSION:Inhibition of lncRNA LINC01503 inhibits the viability,migration and invasion of lung cancer cells.The mechanism may be related to the targeted regulation of miR-335-5p.