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Glabridin induces apoptosis and cell cycle arrest in oral cancer cells through the JNK1/2 signaling pathway
Author(s) -
Chen ChangTai,
Chen YiTzu,
Hsieh YiHsien,
Weng ChiaJui,
Yeh JungChun,
Yang ShunFa,
Lin ChiaoWen,
Yang JiaSin
Publication year - 2018
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22555
Subject(s) - apoptosis , chemistry , cell growth , kinase , cancer cell , signal transduction , microbiology and biotechnology , mapk/erk pathway , pharmacology , biochemistry , biology , cancer , genetics
Glabridin, a flavonoid extracted from licorice ( Glycyrrhiza glabra ), possesses various biological properties, including anticancer activities. However, the effect of glabridin on oral cancer cell apoptosis and the underlying molecular mechanisms has not been elucidated. In this study, we demonstrated that glabridin treatment significantly inhibits cell proliferation in human oral cancer SCC‐9 and SAS cell lines. Flow cytometric assays demonstrated that glabridin induced several features of apoptosis, such as sub‐G1 phase cell increase and phosphatidylserine externalization. Furthermore, glabridin induced apoptosis dose‐dependently in SCC‐9 cells through caspase‐3, −8, and −9 activation and poly (ADP‐ribose) polymerase cleavage. Moreover, glabridin increased the phosphorylation of the extracellular signal–regulated kinase, p38, and c‐Jun N‐terminal kinase (JNK) pathways in a dose‐dependent manner. Moreover, the inhibition of the JNK1/2 inhibitor significantly reversed the glabridin‐induced activation of the caspase pathway. In conclusion, our findings suggest that glabridin induces oral cancer cell apoptosis through the JNK1/2 pathway and is a potential therapeutic agent for oral cancer.