miR-4513 promotes the proliferation and metastasis of non-small cell lung cancer cells by targeting VIPR1

Objectives The pathogenesis of non-small cell lung cancer (NSCLC) is complex. This research focuses on the expression, function, and molecular mechanisms of miR-4513 in NSCLC. Method A total of 126 matched tissue pairs (NSCLC and adjacent normal) were collected, along with assessment of miR-4513 and VIPR1 expression in multiple cell lines (A549, H1299, BEAS-2B) by qRT-PCR. In vitro, the influence of miR-4513 on cellular phenotypes was assessed by determining proliferation rates through CCK-8 assay and quantifying migration/invasion capacities via Transwell systems. Targetscan predicted the targeting relationship between miR-4513 and VIPR1, which was subsequently confirmed by dual-luciferase. Results The expression of miR-4513 is upregulated in NSCLC tissues. The high expression of miR-4513 is associated with pathological features. Survival analysis revealed that high expression of miR-4513 was an independent predictor of unfavorable clinical outcomes in NSCLC patients. In vitro, overexpression of miR-4513 can promote the proliferation, migration and invasion of NSCLC cells, while inhibition of its expression has the opposite effect. VIPR1 overexpression significantly inhibited the proliferation and invasion of NSCLC cells, confirming its tumor-suppressive role. Furthermore, miR-4513 can directly bind to the 3’UTR region of the VIPR1 gene and show a negative correlation with it. Conclusions High expression of miR-4513 may serve as a potential biomarker for poor prognosis in NSCLC patients. In addition, miR-4513 may promote the malignant progression of NSCLC by targeting VIPR1.