Abstract: To explore the molecular mechanism of glabridin-induced B16F10 cell proliferation inhibition via in vitro and in vivo model of melanoma.Glabridin induced B16F10 cell proliferation inhibition and cell apoptosis in a dose-dependent manner. The Bax mRNA and protein expressions were up-regulated and the Bcl-2 was down-regulated in glabridin-treated B16F10 cells. Further studies showed that glabridin decreased the production of ATP and lactic acid in mouse melanoma B16F10 cells. Glabridin down-regulated the mRNA and protein expressions of glycolysis-related kinase genes(Hk2 and Ldha) in B16F10 cells. In addition,the animal model of mouse melanoma indicated that glabridin treatment suppressed tumor growth and induced tumor apoptosis.Both the mRNA and protein levels of glycolysis-related kinase genes(Hk2 and Ldha) and Bcl-2 in tumor tissue were also decreased and Bax was increased in glabridin treated mice. It was concluded thatglabridin inhibited the proliferation and induced apoptosis of melanoma B16F10 cells in a dose-dependent manner,and the inhibition of glycolysis played a crucial role in the induction of apoptosis in glabridin-treated B16F10 cells.

Key words: glabridin, B16F10 cells, glycolysis, apoptosis