LncRNA GAS6-AS1 enhances the progression of pediatric neuroblastoma by modulating miR-3200-3p

BACKGROUND: Neuroblastoma, a highly malignant and heterogeneous tumor, is the most frequent extracranial solid malignancy in children. PURPOSE: This study explores the prognostic significance and biological role of GAS6-AS1 in neuroblastoma, aiming to identify novel biomarkers that could enhance the understanding of disease progression. METHODS: RT-qPCR was used to measure GAS6-AS1 expression levels in neuroblastoma tissues. The association between GAS6-AS1 expression and clinical features was assessed using the chi-square test, while its prognostic impact was examined via Cox regression and Kaplan-Meier survival analysis. Functional experiments, including CCK-8, colony formation, and flow cytometry, were conducted to assess how GAS6-AS1 knockdown influences neuroblastoma cell proliferation and apoptosis. Additionally, Transwell assays evaluated its role in cell migration and invasion. Bioinformatics analysis and dual-luciferase reporter assays were employed to investigate downstream regulatory mechanisms. RESULTS: Elevated GAS6-AS1 expression was observed in neuroblastoma tissues and associated with adverse clinicopathological characteristics. Survival analysis revealed that high GAS6-AS1 levels independently predicted poorer outcomes. Functional assays revealed that GAS6-AS1 depletion attenuated oncogenic behaviors, including proliferation and metastatic potential. Further investigation identified miR-3200-3p as a downstream target of GAS6-AS1, where its suppression counteracted the inhibitory effects of GAS6-AS1 knockdown on malignant phenotypes. Moreover, the results of GO and KEGG analyses indicated that the involvement of the GAS6-AS1/miR-3200-3p axis in neuroblastoma progression may be related to protein polyubiquitination, MAP kinase activity, and autophagy. CONCLUSIONS: This study establishes GAS6-AS1 as a promising prognostic biomarker in neuroblastoma. GAS6-AS1 exerts oncogenic effects by modulating miR-3200-3p, thereby promoting neuroblastoma progression through enhanced malignant phenotypes.