Integrated network pharmacology and experimental models uncover the mechanism of procyanidin B2 against ovarian carcinoma via EGFR/AKT pathway.

Ovarian carcinoma (OC) remains a lethal malignancy with limited therapeutic options. Procyanidin B2, a natural flavonoid, has demonstrated broad bioactivity, yet its potential role in ovarian cancer remains incompletely understood. This study employed an integrated approach combining network pharmacology, molecular docking, and experimental validation to elucidate the anti-tumor mechanisms of Procyanidin B2 in ovarian cancer. Through multi-database screening, 97 potential targets of Procyanidin B2 related to OC were identified. Functional enrichment analyses highlighted significant involvement in cancer-related pathways such as PI3K-Akt, HIF-1 and EGFR tyrosine kinase inhibitor resistance. Protein-protein interaction network analysis identified 10 hub genes, among which EGFR and AKT1 were prioritized. Molecular docking confirmed strong binding interactions between Procyanidin B2 and these targets, particularly EGFR. In vitro assays revealed that Procyanidin B2 selectively inhibited proliferation and colony formation, and induced apoptosis in A2780 and SKOV3 cells, accompanied by upregulation of cleaved caspase-3 and suppression of phosphorylated EGFR and AKT. In a xenograft model, Procyanidin B2 administration significantly suppressed tumor growth without evident toxicity, consistent with the in vitro signaling alterations. These results suggest that Procyanidin B2 exerts anti-ovarian cancer effects partly through modulating the EGFR/AKT signaling axis, supporting its potential as a complementary therapeutic candidate.