Bilobol inhibits the lipopolysaccharide-induced expression and distribution of RhoA in HepG2 human hepatocellular carcinoma cells.

Recent studies have revealed the localization of RhoA protein in the cell nucleus, in addition to its distribution in the cytosol and cell membrane. The results of previous studies by our group indicated that nuclear RhoA expression is increased, or RhoA is transported into the nucleus, when cells become cancerous or damaged. Furthermore, application of the anticancer agent Taxol appeared to reduce nuclear RhoA localization, indicating an association between the nuclear translocation of RhoA and tumor progression. Bilobol is a traditional Chinese medicine ingredient, however, its anticancer effect has remained unclear. The present study aimed to demonstrate the anticarcinogenic action of bilobol against hepatocellular carcinoma, in order to lay the foundations for subsequent research into the mechanisms underlying its anticancer effects. In the present study, HepG2 cells were treated with lipopolysaccharide (LPS), to induce inflammation, and/or bilobol. By performing an ELISA, it was observed that bilobol was able to suppress the inflammation induced by LPS. In addition, immunofluorescence and western blot analyses indicated that bilobol may reduce the expression of RhoA, suppress translocation of RhoA into the nucleus and inhibit the RhoA/Rho-associated protein kinase signaling pathway. In conclusion, the present study revealed the potential anticancer effects of bilobol.