Abstract: To screen out the potential targets and molecular mechanisms of Epigallocatechin gallate (EGCG) in the treatment of triple negative breast cancer (MDA-MB-231). Databases were used to explore the potential targets between EGCG and MDA-MB-231. The “target-pathway” networks of common targets were constructed using Cytoscape 3.8.0 software, while the String database was used to draw and analyze the PPI network. Subsequently, the core genes were submitted to the Metascape database for GO and KEGG enrichment analyses, the prediction results were verified through in vitro experiment. A total of 537 EGCG targets and 181 disaster targets were obtained, 30 key targets were retained by further screening from 88 common potential targets. The results of the enrichment analyses showed that the active targets were involved in 20 core GO biological processes and 17 KEGG signaling pathways. such as cancer signaling pathways, toxic tolerance pathways, pancreatic cancer pathways, rectal cancer pathways, small cell lung cancer pathways. Molecular docking illuminated that EGCG could interact with β-catenin in a non-covalent manner. The in vitro experiment revealed that HGF could induce the expression of β-catenin, and EGCG could repress the HGF-induced over-expression of β-catenin. EGCG inhibited cell viability through multiple targets and multiple pathways, so it has been basically confirmed that EGCG can affect the HGF / β-catenin pathway, providing a theoretical and practical basis for further mechanism exploration.