ArticleDiscover oncology2025
Systematically investigate the mechanism underlying the therapeutic effect of emodin in treatment of prostate cancer.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo systematically investigate the mechanism underlying the therapeutic effect of emodin in treatment of prostate cancer.
methodsCombine network pharmacology, molecular docking, molecular dynamics and experimental verification to explored the mechanism. Using the network pharmacology method, through the TCMSP, DisGeNET and Genecards database, the corresponding targets and related signaling pathways of emodin were screened, and emodin and core targets were studied by molecular docking and molecular dynamics uasing Cytoscape 3.7.2 and other software. The biological processes, cellular components and molecular functions of the key targets were determined by GO enrichment analysis. KEGG enrichment analysis identified signaling pathways associated with key targets. GEPIA and Kaplan-Meier database were used to determine the relationship between the expression of core genes in normal people and prostate cancer patients and the prognosis of patients. Cell proliferation inhibition experiment was carried out by MTT method. The mRNA and protein levels of CASP3, TNF, IL1B, TP53, PPARG, and MYC in PC-3 cells were evaluated by RT-PCR and WB method respectively.
resultsThere were 31 common targets which closely related to emodin in the treatment of prostate cancer. PPI network analysis showed that MYC, PPARG, TP53, TNF, CASP3, IL1B were the core targets. Go and KEGG enrichment analysis showed that pathways in cancer and IL-17 signaling pathway were the key pathways. Molecular docking and molecular dynamics results indicated that emodin had good binding to prostate cancer and 6 core proteins, and the binding force with TP53 protein was the strongest and most stable. The expression of CASP3 protein in normal people was stronger than that in patients with prostate cancer, and the expression of TP53 protein was closely related to the survival rate of patients with prostate cancer. Experimental verification result revealed that EM significantly increased mRNA expressions of CASP3, PPARG and decreased protein expressions of TNF, TP53, MYC at concentrations ranging from 0.1 to 1.6 μmol/L. Emodin significantly increased protein expressions of CASP3, PPARG and decreased protein expressions of TNF, TP53, MYC, IL1B at concentrations ranging from 10 to 160 µmol/L.
conclusionEmodin and TP53 have the best binding and stable conformation among core genes. Emodin exhibits a significant inhibitory effect on PC-3 cells at concentration 0.4 ~ 1.6 μmol/L. It showed that anti-prostate cancer properties by regulating cancer and 1L-17 signaling pathway through up-regulating the expressions of CASP3, PPARG genes/proteins, down-regulating IL1B, TP53, TNF, MYC genes/proteins.
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