Long noncoding RNAs (lncRNAs) and mRNAs (messenger RNAs) have been reported to exert function in non-small-cell lung cancer (NSCLC), but how lncRNAs and mRNAs operate in the regulation of NSCLC is unclear. The purpose of this research was to elucidate the functional mechanism of lncRNA metastasis associated in lung adenocarcinoma transcript 1 () and tripartite-motif protein family member 65 () in NSCLC. Quantitative real-time polymerase chain reaction and western blot assay were employed to measure gene expression. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis were performed to assess cell proliferation and apoptosis, respectively. Also, cell migratory... More
Long noncoding RNAs (lncRNAs) and mRNAs (messenger RNAs) have been reported to exert function in non-small-cell lung cancer (NSCLC), but how lncRNAs and mRNAs operate in the regulation of NSCLC is unclear. The purpose of this research was to elucidate the functional mechanism of lncRNA metastasis associated in lung adenocarcinoma transcript 1 () and tripartite-motif protein family member 65 () in NSCLC. Quantitative real-time polymerase chain reaction and western blot assay were employed to measure gene expression. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis were performed to assess cell proliferation and apoptosis, respectively. Also, cell migratory and invasive abilities were detected by transwell assay. The interaction between and or was predicted by starBase and then confirmed with the dual luciferase reporter assay, RNA immunoprecipitation (RIP) assay, or pull-down assay. Besides, mouse xenograft was conducted to analyze the effect of knockdown on tumor growth . and expression was upregulated, and expression was downregulated in NSCLC tissues and cells. Both knockdown and depletion suppressed cell proliferation, migration, and invasion and induced apoptosis in NSCLC cells. Interestingly, directly inhibited expression and decreased level through interaction. knockdown repressed NSCLC cell growth via modulation of miR-515-5p/ axis. Furthermore, silencing inhibited tumor growth . Our findings demonstrated that depletion inhibited the growth of NSCLC cells by regulating miR-515-5p/ axis, providing the theoretical basis for the therapy of NSCLC.
