Bisphenol S promotes the progression of prostate cancer by regulating the expression of COL1A1 and COL1A2

Abstract

In recent decades, Bisphenol S (BPS), which was once thought to be an alternative for Bisphenol A (BPA) has been extensively used in personal care products, paper products, and food. However, there is an unclear association between bisphenol and tumors. Therefore, clarifying this relationship is critical for disease prevention and treatment. This work found a novel method that predicts a correlation between bisphenol interactive genes and tumors. First, the transcriptome profile and interactive genes of bisphenol were obtained from The Cancer Genome Atlas and Genotype-Tissue Expression, Comparative Toxicology Genomics, and PharmMapper databases. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis revealed that interactive genes are primarily enriched in prostate cancer. Gene targeted prediction and gene set variation analysis confirmed that bisphenol exerts potential effects on prostate cancer. The operating characteristic curves and survival analysis uncovered the role of COL1A1 and COL1A2 in predicting the prognosis of prostate cancer. Cell counting kit-8 assay revealed that BPS-treated cells could remarkably promote cell proliferation capacity in both PC-3 and LNCap cells. In addition, wound healing and transwell assays demonstrated that BPS-treated cells could significantly promote the cell invasion capacity of prostate cells. Notably, two key genes, i.e., COL1A1 and COL1A2 were significantly upregulated with BPS-treated PC-3 and LNCap cells.