Bioinformatics identification of key genes and pathways for neural stem cells

Objective: Neural stem cells (NSCs) hold promise for treating neurological disorders due to their self-renewal and differentiation capacities. However, the molecular mechanisms underlying NSC function remain insufficiently defined. This study aimed to systematically identify NSC-specific targets and elucidate their functional networks using bioinformatics approaches. Methods: NSC-related targets were retrieved from the GeneCards database and filtered by relevance scores. Protein-protein interaction (PPI) networks were constructed through the STRING database and analyzed in Cytoscape with the cytoHubba plugin using the maximal clique centrality algorithm to identify hub genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed using the DAVID platform. A “key targets-KEGG pathways” network was subsequently built to integrate hub targets with enriched signaling pathways. Results: A total of 155 NSC-associated targets were identified, from which 10 hub genes were highlighted, primarily subunits of the SWI/SNF (BAF) chromatin remodeling complex, including SWI/SNF related BAF chromatin remodeling complex subunit ATPase 4/2 (SMARCA4/2), and AT-Rich interaction domain 1A/B (ARID1A/B). GO enrichment analysis revealed significant involvement in apoptosis regulation, neuron fate specification, chromatin remodeling complexes, and transcription factor binding. KEGG pathway analysis identified 22 enriched pathways, with the top 10 including ATP-dependent chromatin remodeling, stem cell pluripotency, PI3K-Akt signaling, thermogenesis, synaptic vesicle cycle, and neurodegeneration-related pathways. The integrated “key targets-KEGG pathways” network demonstrated that hub genes were central regulators linking chromatin remodeling to cancer-related and stemness-associated pathways. Conclusion: This bioinformatics analysis highlights chromatin remodeling as a central mechanism regulating NSC biology, with SWI/SNF complex subunits emerging as key hub targets. The identified pathways underscore the interplay between transcriptional regulation, metabolic reprogramming, and stemness maintenance, providing insights into NSC function and potential therapeutic strategies for neurological disorders and regenerative medicine.