Isoliquiritigenin Induces Autophagy and Inhibits Ovarian Cancer Cell Growth
AbstractOvarian cancer is one of the commonest gynecologic malignancies, which has a poor prognosis for patients at the advanced stage. Isoliquiritigenin (ISL), an active flavonoid component of the licorice plant, previously demonstrated antioxidant, anti-inflammatory, and tumor suppressive effects. In this study, we investigated the antitumor effect of ISL on human ovarian cancer in vitro using the human ovarian cancer cell lines, OVCAR5 and ES-2, as model systems. Our results show that ISL significantly inhibited the viability of cancer cells in a concentration- and time-dependent manner. Flow cytometry analysis indicated that ISL induced G2/M phase arrest. Furthermore, the expression of cleaved PARP, cleaved caspase-3, Bax/Bcl-2 ratio, LC3B-II, and Beclin-1 levels were increased in western blot analysis. To clarify the role of autophagy and apoptosis in the effect of ISL, we used the autophagy inhibitor—3-methyladenine (3-MA) to attenuate the punctate fluorescence staining pattern of the p62/sequestosome 1 (SQSTM1, red fluorescence) and LC3 (green fluorescence) proteins after ISL treatment, and 3-MA inhibited the cytotoxicity of ISL. These findings provide new information about the link between ISL-induced autophagy and apoptosis and suggest that ISL is a candidate agent for the treatment of human ovarian cancer. View Full-Text
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Chen, H.-Y.; Huang, T.-C.; Shieh, T.-M.; Wu, C.-H.; Lin, L.-C.; Hsia, S.-M. Isoliquiritigenin Induces Autophagy and Inhibits Ovarian Cancer Cell Growth. Int. J. Mol. Sci. 2017, 18, 2025.
Chen H-Y, Huang T-C, Shieh T-M, Wu C-H, Lin L-C, Hsia S-M. Isoliquiritigenin Induces Autophagy and Inhibits Ovarian Cancer Cell Growth. International Journal of Molecular Sciences. 2017; 18(10):2025.Chicago/Turabian Style
Chen, Hsin-Yuan; Huang, Tsui-Chin; Shieh, Tzong-Ming; Wu, Chi-Hao; Lin, Li-Chun; Hsia, Shih-Min. 2017. "Isoliquiritigenin Induces Autophagy and Inhibits Ovarian Cancer Cell Growth." Int. J. Mol. Sci. 18, no. 10: 2025.
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