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Estrogen receptor-positive breast cancer (ERPBC) is the commonest subtype of breast cancer, with a high prevalence, incidence, and mortality. Herbal drugs are increasingly being used to treat ERPBC, although their mechanisms of action are not fully understood. Therefore, in this study, we aimed to analyze the therapeutic properties of FDY003, a herbal anti-ERPBC prescription, using a network pharmacology approach. FDY003 decreased the viability of human ERPBC cells and sensitized them to tamoxifen, an endocrine drug that is widely used in the treatment of ERPBC. The network pharmacology analysis revealed 18 pharmacologically active components in FDY003 that may interact with and regulate 66 therapeutic targets. The enriched gene ontology terms for the FDY003 targets were associated with the modulation of cell survival and death, cell proliferation and growth arrest, and estrogen-associated cellular processes. Analysis of the pathway enrichment of the targets showed that FDY003 may target a variety of ERPBC-associated pathways, including the PIK3-Akt, focal adhesion, MAPK, and estrogen pathways. Overall, these data provide a comprehensive mechanistic insight into the anti-ERPBC activity of FDY003.

natural product communications

Network Pharmacology-Based Dissection of the Comprehensive Molecular Mechanisms of the Herbal Prescription FDY003 Against Estrogen Receptor-Positive Breast Cancer