Glabridin Induces Apoptosis in Human Oral Cancer Cells

Objectives: Oral cancer is the fourth leading cause of cancer death and is associated with increasing morbidity and mortality rates in Taiwan. Glabridin, a flavonoid extracted from licorice, owns a variety of biological properties including anti-cancer activities. Glabridin exhibits anti-tumor functions in that it attenuates the proliferation, migration, invasion, and angiogenesis of human cancer cells. However, the effect of glabridin on oral cancer cells apoptosis and the underlying molecular mechanisms have not been elucidated yet.
Methods: SCC-9 and SAS cells were used to investigate the cell viabilities treated by glabridin through MTT assays. The expressions of apoptosis-related and MAPK pathway proteins have been determined using western blot analysis.
Results: The results showed that glabridin significantly inhibited cell proliferation in human oral cancer cell lines. Furthermore, glabridin induced apoptosis dose-dependently in SCC9 cells through caspases-3, -8, and -9 activations and PARP cleavage. Moreover, glabridin also increase phosphorylation of ERK1/2, p38 MAPK and JNK1/2 in dose-dependent manner. The inhibition of p38 MAPK and JNK1/2 by specific inhibitors significantly reduced the glabridin-induced activation of the caspase-3, -8 and -9.
Conclusions: Taken together, our findings suggest that glabridin induced SCC9 cell apoptosis through p38 MAPK and JNK1/2 pathways and could serve as a potential chemotherapeutic agent for the treatment of oral cancer.