ArticleWorld journal of surgical oncology2026
LncRNA GAS6-AS1 enhances the progression of pediatric neuroblastoma by modulating miR-3200-3p.
Article in World journal of surgical oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
backgroundNeuroblastoma, 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.
methodsRT-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.
resultsElevated 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.
conclusionsThis 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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.