Inhibitory effect of glucocorticoid on proliferation of human hepatoma carcinoma cell line in vitro

Abstract

Objective To illustrate the role of glucocorticoids in growth regulation of human hepatoma cells and the possible mechanism. Methods The human hepatoma carcinoma cell lines Be17402, H7402 and Hep G2 were treated with different concentrations of dexamethasones (Dex) (0.1, 0.01, 1×10-3, 1×10-4, 1×10-5, and 1×10-6 mmol/L). The inhibition rate was calculated. Be17402 cells were treated with Dex (1×10-4 mmol/L, Dex group), or RU486 (1×10-4 mmol/L, RU486 group) or both (both concentrations were 1×10-4 mmol/L, Dex+ Ru486 group), or medium as negative control group. The inhibition rate was calculated, and the cycle progression was measured by flow cytometry. Western blot was used to detect the expression of P21 protein, and the reporter genes were employed to detect the effect of Dex and Ru486 on promoter of NF-kappa B in Be17402 cells. Results Dex could significantly inhibit the proliferation of these cells in a dose-dependent manner. Dex inhibited the growth of Be17402, and induced G0/G1 arrest. Dex increased the expression of P21, and suppressed the promoter of NF-kappa B. Ru486 could reverse these effects. Conclusion Up-regulation of P21/WAF1 expression and suppression of promoter of NF-κB may contribute to the growth inhibition and G0/G1 arrest induced by glucocorticoid in human hepatoma carcinoma cells. These effects may be mediated by GR. Key words: Carcinoma, hepatocellular; Glucocortieoids; Cell proliferation