A novel strategy for the study on molecular mechanism of prostate injury induced by 4,4′-sulfonyldiphenol based on network toxicology analysis

The study aimed to investigate the underlying molecular mechanisms of prostate injury induced by 4,4 & PRIME;-sulfonyldiphenol (BPS) exposure and propose a novel research strategy to systematically explore the molecular mechanisms of toxicant-induced adverse health effects. By utilizing the ChEMBL, STITCH, and GeneCards databases, a total of 208 potential targets associated with BPS exposure and prostate injury were identified. Through screening the potential target network in the STRING database and Cytoscape software, we determined 21 core targets including AKT1, EGFR, and MAPK3. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses conducted through the DAVID database illustrated that the potential targets of BPS in prostatic toxicity were primarily enriched in cancer signaling pathways and calcium signaling pathways. These findings suggest that BPS may actively participate in the occurrence and development of prostate inflammation, prostatic hyperplasia, prostate cancer, and other aspects of prostate injury by regulating prostate cancer cell apoptosis and proliferation, activating inflammatory signaling pathways, and modulating prostate adipocytes and fibroblasts. This research provides a theoretical basis for understanding the molecular mechanism of underlying BPS-induced prostatic toxicity and establishes a foundation for the prevention and treatment of prostatic diseases associated with exposure to plastic products containing BPS and certain BPS-overwhelmed environments.

Automated summary

The study identified 208 potential targets associated with 4,4'-sulfonyldiphenol (BPS) exposure and prostate injury using databases such as ChEMBL, STITCH, and GeneCards. Through network screening, 21 core targets including AKT1, EGFR, and MAPK3 were determined. Gene ontology and KEGG pathway analysis revealed that the potential targets of BPS were enriched in cancer signaling pathways and calcium signaling pathways. These findings suggest that BPS actively participates in prostate injury by regulating cancer cell apoptosis and proliferation, activating inflammatory signaling pathways, and modulating prostate adipocytes and fibroblasts.