Objective: Polycystic ovary syndrome (PCOS) is the most common endocrine disorder among reproductive-age women, with a prevalence of 6–13%. The precise molecular network structure and central driver genes in PCOS pathogenesis remain incompletely understood.

Method: A total of 200 differentially expressed genes linked to PCOS were retrieved from multiple transcriptomic studies. Protein-protein interaction (PPI) networks were constructed using the STRING database (confidence score >0.40) and further analyzed in Cytoscape version 3.10.2. Hub genes were identified by CytoHubba plugin based on degree, betweenness, and closeness centrality measures. Pathway enrichment analysis was conducted using KEGG, Gene Ontology, Reactome, and WikiPathways databases; only terms with FDR <0.05 were considered significant.

Results: The resulting network consisted of 200 nodes and 4,979 edges. Four core genes—PIK3CA, PIK3CD, AKT1, and PIK3CB—were present in all eight highly dysregulated pathways (PI3K-Akt, AMPK, longevity regulating, AGE-RAGE, FoxO, insulin resistance, HIF-1, and TNF signaling), with PI3K-Akt showing the strongest enrichment (29 genes, FDR=3.28×10⁻¹â°). Three additional biomarkers (INSR, INS, IL6) overlapped in six pathways.

Conclusions: PIK3CA, PIK3CD, AKT1, and PIK3CB emerge as central molecular hubs and promising therapeutic targets in PCOS. Extensive pathway convergence on these nodes highlights the systemic metabolic-inflammatory basis of the disorder.