LINC01093 promotes proliferation and invasion of non-small cell lung cancer cells via targeting akt signaling pathway.

Abstract

To explore the expression of LINC01093, a long non-coding ribonucleic acid (lncRNA) in non-small cell lung cancer (NSCLC) tissues, and cells and its regulatory role in NSCLC cell proliferation and invasion. The expression of LINC01093 in NSCLC tissues and cells was detected via quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) experiment. The specific sequences interfering in LINC01093 were designed and transiently transfected into A549 and SPCA-1 cells using LipofectamineTM 2000, and 48 later, the transfection efficiency was detected. Moreover, the impacts of small interfering (si)-LINC01093 on NSCLC cell proliferation were observed via methyl thiazolyl tetrazolium (MTT) and colony forming assays, the influence of LINC01093 on the cycle distribution of NSCLC cells was determined through flow cytometry, and the changes in the invasion and migration abilities of NSCLC cells were evaluated via transwell assay after interfering in the expression of LINC01093. Finally, the expression changes of the molecular markers in the protein kinase B (Akt) signaling pathway in the downstream of LINC01093 were detected via Western blotting. According to the results of qRT-PCR, the relative expression level of LINC01093 was up-regulated in NSCLC tissues and cells. After interfering in the expression of LINC01093, the results of MTT and colony forming assays revealed that the proliferation ability of NSCLC cells was weakened, according to the findings in the flow cytometry, the cells were arrested in G1/0 phase, the transwell assay results manifested that the cell migration and invasion abilities were weakened, and the results of the Western blotting suggested the changes in the expressions of molecular markers in the Akt signaling pathway. The expression of LINC01093 is upregulated in NSCLC tissues and cells, and it facilitates the proliferation, invasion, and metastasis of NSCLC cells via the Akt signaling pathway.