ArticleAmerican journal of translational research2025
lncRNA SYNPR-AS1 promotes non-small cell lung cancer progression by the microRNA-3619-5p/FOXK1 axis.
Article in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo examine SYNPR-AS1 expression in non-small cell lung cancer (NSCLC) and evaluate its biological effects on cancer progression.
methodsSYNPR-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.
resultsSYNPR-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.
conclusionsSYNPR-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.
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