Campesterol induces apoptosis and inhibits proliferation in HepG2 liver cancer cells

Aim of the study: Hepatocellular carcinoma (HCC) is the most common primary liver malignancy and a leading cause of cancer-related mortality worldwide.Despite advances in therapy, the prognosis remains poor, highlighting the need for novel, low-toxicity therapeutic strategies.Campesterol, a naturally occurring dietary phytosterol, has been reported to exert anti-proliferative and pro-apoptotic effects in various cancers, yet its activity in liver cancer cells remains underexplored. Material and methods:The anticancer potential of campesterol was evaluated in human hepatocellular carcinoma (HepG2) cells.Cells were treated with increasing concentrations of campesterol (10, 50, 100, and 200 µg/ml) for 24 h.Cell viability and proliferation were assessed by MTT and crystal violet assays, while cell death was quantified by trypan blue exclusion.Data were analysed using one-way ANOVA followed by Tukey's post-hoc test, with p < 0.05 considered significant.Results: Campesterol exhibited a dose-dependent effect on HepG2 cells.No significant change in viability was observed at lower concentrations (10-100 µg/ml), whereas a marked reduction in cell viability and increase in cell death were detected at 200 µg/ml (p < 0.05).Findings were consistent across MTT, crystal violet, and trypan blue assays, supporting the concept of apoptosis-associated cytotoxicity.Conclusions: These findings demonstrate that campesterol reduces viability and promotes apoptosis in HepG2 cells, suggesting its potential as a low-toxicity adjunct in HCC therapy.Further mechanistic investigations and in vivo studies are warranted to validate its translational applicability.