miR-486-5p functions as an oncogene by targeting PTEN in non-small cell lung cancer.

Purpose: Lung cancer, the leading cause of cancer-related death worldwide, shows a poor 5-year overall survival rate. In our previous study, we demonstrated that miR-486-5p can be a potential blood-based biomarker for early diagnosis and recurrence prediction of non-small cell lung cancer (NSCLC). The aim of the present study was to investigate the possible roles and related target genes of miR-486-5p in NSCLC progression.

Methods: pcDNA3.1(+)/Pri-miR486 recombinant plasmid and miR-486-5p inhibitor were transfected into NSCLC cells and theirs effects were evaluated by qRT-PCR. Then, MTT assay and Colony formation assay were performed to determine the potential roles of miR-486-5p played on NSCLC cellular proliferation and cloning in vitro. We also initially investigated the target genes of miR-486-5p by using bioinformatic methods, qRT-PCR and western blot.

Results: pcDNA3.1(+)/Pri-miR486 recombinant plasmid significantly upregulated the expression of miR-486-5p, while miR-486-5p inhibitor significantly downregulated its expression. Upregulation of miR-486-5p promoted the cellular proliferation and cloning, while miR-486-5p silencing restrained the cellular proliferation and cloning. Furthermore, four potential target genes (PIK3R1, PTEN, MAP3K7 and FOXO1) of miR-486-5p were screened out. Finally, we found that upregulation of miR-486-5p in NSCLC cells significantly reduced PTEN and increased AKT expression levels, whereas miR-486-5p silencing increased PTEN and reduced AKT expression. Therefore, we believe that miR-486-5p can regulate PTEN-PI3 K/AKT signaling.

Conclusions: miR-486-5p acts as an oncogene in the progression of NSCLC by influencing PTEN-PI3 K/AKT signaling. miR-486-5p may provide potential therapeutic targets for NSCLC.