Dysregulated Contributes to the Vitality and Migration of NSCLC Via miR-19a-3p/miR-19b-3p/miR-125b-5p.

Accumulating evidence implies that long noncoding RNAs participate in non-small cell lung cancer (NSCLC) tumorigenesis. Our current study synthetically analyzed RNA sequencing data downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. We identified significantly downregulated in NSCLC tissues. We explored the expression in NSCLC tumor tissues and cell lines with reverse transcription-quantitative polymerase chain reaction analysis. Lentivirus-mediated infection upregulated the expression of in A549 cells. The proliferation and migration capability were also measured in A549 cells. In addition, we performed luciferase reporter gene assay to investigate whether directly interacts with miR-19a-3p/miR-19b-3p/miR-125b-5p. A nude mice model was used to detect the potential biological process of on tumor growth . The results showed that was significantly down-egulated in NSCLC tissues and cell lines. LV-LINC00961 effectively increased the expression of and decreased the expression of miR-19a-3p/miR-19b-3p/miR-125b-5p. upregulation remarkably inhibited cell proliferation, migration, and invasion while promoting cell apoptosis in A549 cells. Luciferase reporter gene assay revealed that could directly sponge miR-19a-3p/miR-19b-3p/miR-125b-5p. Moreover, overexpressed miR-19a-3p/miR-19b-3p/miR-125b-5p reversed the effect of on cell function of A549 cells. Western blot assays revealed that could partially act as a tumor suppressor via affecting PI3K-AKT/MAPK/mTOR signaling pathway. In addition, overexpressed -inhibited tumor growth was demonstrated . Overexpression of inhibited cell viability, invasion, and induced apoptosis in NSCLC, potentially via suppressing the expression of miR-19a-3p/miR-19b-3p/miR-125b-5p by targeting PI3K-AKT/MAPK/mTOR signaling pathways, which might provide the potential biomarker for NSCLC diagnosis and therapies.