1. Study on the potential mechanism of Pu Gong Ying in treating breast hyperplasia based on network pharmacology and molecular docking.
- Author
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Zhiyong Sun, Shuli Gao, Yang Zhang, Gangqiang Xue, Zilin Yuan, and Shaonan Wang
- Subjects
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MOLECULAR pharmacology , *MOLECULAR docking , *HYPERPLASIA , *PROTEIN-protein interactions , *CELLULAR signal transduction - Abstract
In the present study, network pharmacology was employed to elucidate the targets and pathways involved in the treatment of breast hyperplasia (BH) by Pu Gong Ying (PGY). Molecular docking was utilized to analyze the interaction between PGY and key targets based on the findings of network pharmacology. The intersection of 261 targets associated with 15 PGY compounds and 2455 targets related to BH yielded 90 common targets (89 of which were included in the protein-protein interaction (PPI) network, while one target did not exhibit interactions with any other targets in the PPI network). The top 10 hub targets ranked in the PPI network and the top 10 targets according to the Molecular Complex Detection (MOCDE) score were intersected, resulting in the identification of CASP3, EGFR, ESR1, ERBB2, MMP9, and PTGS2 as key targets, as determined by different algorithms. Gene Ontology (GO) functional enrichment analysis revealed 284 biological components. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis identified 125 pathways, primarily associated with the regulation of pathways in cancer, the PI3K-Akt signaling pathway, the MAPK signaling pathway, microRNAs in cancer, chemical carcinogenesis-receptor activation, and others. Molecular docking results demonstrated the favorable binding efficacy of PGY9, PGY10, and PGY11 with the core targets. The findings suggested that PGY exerted its therapeutic effects on BH through multiple targets and biological pathways. This study contributed to the understanding of the molecular mechanisms underlying BH development and provided implications for BH-targeted therapy and even breast cancer prevention. [ABSTRACT FROM AUTHOR]
- Published
- 2023
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