LncRNA ASB16-AS1 promotes proliferation and inhibits apoptosis of non small cell lung cancer cells by activating the Wnt/beta catenin signaling pathway.

OBJECTIVE: To detect the expression of long non-coding ribonucleic acid (lncRNA) ASB16-AS1 in non-small cell lung cancer (NSCLC) tissues and cells, and to explore the effect of lncRNA ASB16-AS1 on the biological functions of NSCLC cells. PATIENTS AND METHODS: The expression level of lncRNA ASB16-AS1 in NSCLC tissues and cells was detected via real-time fluorescence quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR). The interference sequences of lncRNA ASB16-AS1 were designed and synthesized, and its transfection efficacy was detected by qRT-PCR. After knockdown of lncRNA ASB16-AS1, the proliferation, cell cycle, and apoptosis of NSCLC cells were detected via cell counting kit-8 (CCK-8) assay, colony formation assay, and flow cytometry, respectively. Moreover, the expression changes in the Wnt/beta catenin signaling pathway were detected via Western blotting. RESULTS: LncRNA ASB16-AS1 was upregulated in NSCLC tissues and cells compared with that in paracarcinoma tissues and 16HBE cells. The results of CCK-8 assay and colony formation assay revealed that the silence of lncRNA ASB16-AS1 attenuated the proliferative ability in NSCLC. The results of flow cytometry manifested that the silence of lncRNA ASB16-AS1 arrested the cell cycle in G0/1 phase, and accelerated the apoptosis rate. The key proteins in the Wnt/beta-catenin signaling pathway were regulated by lncRNA ASB16-AS1 in NSCLC. CONCLUSIONS: LncRNA ASB16-AS1 is upregulated in NSCLC tissues and cells, which promotes proliferation and inhibits apoptosis of NSCLC cells through the Wnt/beta-catenin signaling pathway.