LncRNA MEG8 promotes tumor progression of non-small cell lung cancer via regulating miR-107/CDK6 axis.

Mounting evidence has implicated the vital role of long noncoding RNAs (lncRNAs) in non-small cell lung cancer (NSCLC). This study aims to investigate the mechanism of lncRNA MEG8 on NSCLC progression. The mRNA expressions of MEG8 and miR-107 were examined in tumor and adjacent normal tissues from patients with NSCLC by qRT-PCR. Lung epithelial BEAS-2B cells were transfected with MEG8 overexpression plasmid, and NSCLC A549 and H1299 cells were transfected with MEG8 or miR-107 overexpression/knockdown plasmid to detect the function of MEG8 or miR-107 on cell activity. The function of MEG8 and miR-107 on cell proliferation, cell cycle changes, invasion and migration was separately determined by Cell counting kit-8 assay and 5-ethynyl-2'-deoxyuridine staining, flow cytometry, transwell and cell scratch test. Target sites for miR-107 and MEG8, miR-107 and CDK6 were determined and verified by a dual luciferase gene reporter assay. The expression levels of the Rb/E2F3 signal pathway related proteins (p21, p27, E2F3 and Rb) were inspected by Western blot. MEG8 was strongly expressed while miR-107 was lowly expressed in tumor tissues and cells. Overexpression of MEG8 potentiated cell proliferation, migration and invasion in BEAS-2B cells. Silencing MEG8 or overexpression of miR-107 clearly hindered cell progression in A549 and H1299 cells. Mechanistically, MEG8 and CDK6 can competitively bind to miR-107 and together regulate the progression of NSCLC. Additionally, silencing MEG8 or overexpression of miR-107 can inhibit the phosphorylation levels of Rb and E2F3. Evidence in this work indicated that MEG8 regulates miR-107/CDK6 axis to promote NSCLC progression by activating the Rb/E2F3 pathway.