Conclusion
In conclusion, these findings demonstrated that PCAT18 promoted NSCLC development by sponging miR-4319. PCAT18 may serve as a crucial biomarker for the diagnosis and targeted therapy of NSCLC.
Methods
The PCAT18 expression in NSCLC tissues and cell lines were evaluated by reverse transcription-quantitative PCR. Cell Counting Kit-8 assays, colony formation study, wound healing assays and transwell invasion assays, and tumor xenograft experiments were performed to investigate the biological functions of PCAT18 in NSCLC. Luciferase reporter, RNA-binding protein immunoprecipitation (RIP) and RNA pull-down assays were further used to explore the association between PCAT18 and miR-4319.
Results
PCAT18 expression was up-regulated in NSCLC tissues and cell lines. Furthermore, PCAT18 silencing inhibited NSCLC cell proliferation, migration and invasion, while co-transfection with a miR-4319 inhibitor reversed these biological effects, and miR-4319 inhibited NSCLC growth in vivo. Additionally, PCAT18 silencing promoted NSCLC cell apoptosis and induced G1 stage arrest. Moreover, luciferase reporter assays illustrated that PCAT18 regulated miR-4319 directly, and a RIP assay and RNA pull-down analysis further demonstrated that miR-4319 inhibited PCAT18 in a RNA-induced silencing complex-dependent manner. Finally, PCAT18 silencing impaired the growth of NSCLC in vivo.