Campesterol induces apoptosis and inhibits proliferation in HepG2 liver cancer cells

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.

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.

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.

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.