Anti-tumor Mechanism of Camellia nitidissima Based on Network Pharmacology and Molecular Docking

Background: Modern pharmacological research indicated that Camellia nitidissima (CAM) had significant anti-tumor activity, but the investigation of its mechanism was still lacking. Objective: The multi-component, multi-target and multi-pathway mechanism of CAM against tumor was investigated based on network pharmacology and molecular docking. Methods: The active ingredients and targets of CAM were selected through a literature search, Traditional Chinese Medicine Systems Pharmacology database and PharmMapper database, and tumor-related targets were selected by GeneCards database, then to obtain the anti-tumor related targets of CAM. The protein interaction relationship was obtained through STRING database, protein-protein interaction network was constructed using Cytoscape 3.7.2 software, and enrichment analysis of GO and KEGG was conducted. AutoDock Tools 1.5.6 software was used to verify the molecular docking between the key ingredients and the key targets. Results: Catechin, epicatechin and luteolin were identified as the key anti-tumor related ingredients, and ESR1, EGFR, MAPK8, MAPK10, AR, PGR, F2 and PIK3CG were identified as the key targets. The GO entries mainly involved metabolic process, cellular process, response to stimulus, organelle, cytosol, etc. The KEGG enrichment showed that the key pathways included pathways in cancer, prostate cancer, pancreatic cancer, breast cancer, estrogen signaling pathway, MAPK signaling pathway, PI3K-Akt signaling pathway, etc. KEGG pathway maps indicated that the anti-tumor effect of CAM may be mainly achieved by intervening related targets in the following pathways: AR-HSP/AR-AR/PSA/proliferation and evading apoptosis; F2/GPCR/& mldr;/ROCK/tissue invasion and metastasis; F2/GPCR/& mldr;/Raf/MAPK signaling pathway/proliferation and sustained angiogenesis; EGFR/PI3K-Akt signaling pathway/proliferation, evading apoptosis and sustained angiogenesis; EGFR/Grb2/& mldr;/Raf/MAPK signaling pathway/proliferation and sustained angiogenesis; ER/Estrogen signaling pathway/proliferation; PR/PR-CoR/Wnts-RANKL/proliferation; oxidative stress (.O2-, .OH, H2O2)/KEAP1/NRF2/.../proliferation and evading apoptosis. The results of molecular docking showed that the key active ingredients had a good binding activity with each key target. Conclusion: It was predicted that the main active ingredients of CAM could bind to tumor-related targets, such as receptor and coagulation-promoting factor, scavenge free radicals, and then interfere with the occurrence and development of tumors.