Fenbendazole promotes TP53 activation and selective cancer cell inhibition with limited impact on normal dermal fibroblasts 3665

Abstract Description Introduction Fenbendazole, a benzimidazole carbamate traditionally used as an anthelmintic, has recently shown potential anticancer properties. This study evaluates its cytotoxic effects on cancer cell lines and selectivity by assessing its impact on normal human dermal fibroblasts (HDFa). Methods Cancer cell lines, including breast, prostate, and melanoma, were treated with fenbendazole at varying concentrations. Cell viability was assessed using the Trypan Blue exclusion assay. Quantitative PCR measured TP53 expression post-treatment. Parallel experiments were conducted on HDFa cells. Results Fenbendazole caused a dose-dependent viability decrease across all cancer cell lines. Breast and prostate cells were sensitive at lower doses, while melanoma cells needed higher doses for similar effects. Treated cancer cells showed upregulated TP53 expression, suggesting apoptotic pathway activation. HDFa cells showed minimal viability reduction, suggesting a favorable selectivity profile. Conclusions Fenbendazole effectively inhibits cancer cell proliferation, likely via TP53 activation, while showing minimal cytotoxicity to HDFa cells, warranting further investigation into its therapeutic potential. Topic Categories Tumor Immunology: Checkpoints, Prevention, and Treatment (TIPT)