Mechanistic Exploration and Experimental Validation of Yadanzi Oil in Treating Breast Cancer Based on Network Pharmacology and Molecular Docking Technology

Objective Brucea javanica oil emulsion (Yadanzi oil, BJOE), a traditional Chinese medicine (TCM), is widely used in clinical practice in China, including for the treatment of breast cancer (BC). However, its specific active components and mechanisms of action against BC remain unclear. This study aims to systematically identify the key bioactive compounds of BJOE and decipher their anti-BC mechanisms through an integrative network pharmacology approach combined with experimental validation. Methods Active components and potential targets of Yadanzi were retrieved from the Traditional Chinese Medicine Systems Pharmacology Database (TCMSP). BC-related genes were collected from public databases. A compound-target network was constructed using Cytoscape. Furthermore, protein-protein interaction (PPI) network construction, along with Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, were performed to identify hub targets and signaling pathways. Finally, molecular docking, in vitro and in vivo experiments were performed to verify the network pharmacology results. Results Fifteen active components of Yadanzi were screened from the TCMSP database. After excluding compounds without target information, two key bioactive compounds (beta-sitosterol and luteolin) and 73 potential targets were retained, among which 71 were associated with BC. Network analysis revealed AKT1, CASP3, and TP53 as hub targets. Enrichment analysis indicated these genes are primarily involved in apoptosis regulation, PI3K-Akt signaling, and other cancer-related pathways. Molecular docking demonstrated strong binding affinity between luteolin and AKT1/CASP3/TP53, as well as between beta-sitosterol and CASP3, with binding energies ranging from −6.4 to −7.8 kcal/mol. In vitro experiments verified that luteolin inhibits the proliferation and migration of breast cancer cells and induces apoptosis, reducing viability by up to 50% ( P < .001) and increasing apoptotic rates by approximately 2-fold compared to controls ( P < .001). Western blot analysis indicated that luteolin regulate the expression levels of proteins associated with apoptosis. Xenograft mouse model verified that luteolin could delay tumor growth. Conclusion This study provides a novel network pharmacology-based framework for elucidating the anti-BC mechanisms of BJOE. It was suggested that the key active component luteolin can inhibit BC cell proliferation, induce apoptosis and regulate the expression of related proteins associated with apoptosis. By integrating computational predictions with experimental validation, our work offers deeper insights into the pharmacological basis of BJOE and supports its potential as a complementary therapeutic agent for breast cancer.