Expression of junB is markedly stimulated by glycyrrhizin in a human hepatoma cell line.

Effective therapeutic approaches for liver cancer are expected to be the prevention of chronic inflammation, progression of chronic liver injury to liver cancer and/or tumor cell growth by activating various oncogenes. Activation of the c-jun oncogene occurs in many cases at the early stage of transformation of chronic hepatitis into liver cancer. Accordingly, inhibition of c-jun gene function is thought to be important for the therapy of liver cancer. Although the junB gene has been identified as a c-jun-related gene, it acts as a tumor suppressor gene through competitive binding of JUNB with c-JUN. Therefore, alteration in junB gene expression in chronic hepatitis or liver cancer is an interesting target for the development of both therapeutic treatment and medicines. Monoammonium glycyrrhizinate (MAG) is used for the treatment of viral hepatitis or the prevention of chronic liver diseases. However, the mechanism by which MAG is involved in the suppression of oncogene function has not yet been characterized. In the present study, we first found that MAG highly stimulated JUNB expression in a human hepatoma cell line, HepG2. We examined the mechanism by which MAG increases junB gene expression by considering the previously published effects of MAG on the onset or development of chronic hepatitis or liver injury. The present data suggest that marked activation of junB expression leads to a pivotal role for MAG in multiple medical applications.