lncRNA SYNPR-AS1 promotes non-small cell lung cancer progression by the microRNA-3619-5p/FOXK1 axis.

OBJECTIVE: To examine SYNPR-AS1 expression in non-small cell lung cancer (NSCLC) and evaluate its biological effects on cancer progression. METHODS: SYNPR-AS1 expression levels were quantified using quantitative real-time PCR. Functional experiments were performed to investigate the effects of SYNPR-AS1 on NSCLC cell phenotypes. In addition, the underlying mechanisms of action were explored through bioinformatic analysis, luciferase reporter assays, and RNA immunoprecipitation (RIP) experiments. RESULTS: SYNPR-AS1 was significantly upregulated in NSCLC tissues and cells. Functional experiments confirmed that SYNPR-AS1 knockdown suppressed cell proliferation, migration, and invasion, whereas its overexpression promoted these malignant behaviors. Mechanistically, SYNPR-AS1 competitively interacts with microRNA-3619-5p (miR-3619-5p), thereby preventing miR-3619-5p- mediated repression of Forkhead box protein K1 (FOXK1). Furthermore, rescue experiments confirmed that the inhibitory effects of SYNPR-AS1 knockdown in NSCLC cells were abrogated by miR-3619-5p inhibition or FOXK1 overexpression. CONCLUSIONS: SYNPR-AS1 exerts pivotal functions in NSCLC through decoying miR-3619-5p and thereby regulating FOXK1 expression. The SYNPR-AS1/miR-3619-5p/FOXK1 axis may be an effective target for NSCLC therapy.