Isoliquiritigenin induces apoptosis and autophagy and inhibits endometrial cancer growth in mice

Endometrial cancer is the most common cancer in women, typically with onset after menopause. Isoliquiritigenin (ISL), a licorice flavonoid, was previously shown to have anti-oxidant, anti-inflammatory, and tumor suppression effects. In this study, we investigated the anti-tumor effect of ISL on huma...

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Published in:Oncotarget 2016-11, Vol.7 (45), p.73432-73447
Main Authors: Wu, Chi-Hao, Chen, Hsin-Yuan, Wang, Chia-Woei, Shieh, Tzong-Ming, Huang, Tsui-Chin, Lin, Li-Chun, Wang, Kai-Lee, Hsia, Shih-Min
Format: Article
Language:English
Subjects:
Animals
Antineoplastic Agents, Phytogenic - pharmacology
Apoptosis - drug effects
Autophagy - drug effects
Cell Cycle Checkpoints - drug effects
Cell Line, Tumor
Cell Proliferation - drug effects
Chalcones - pharmacology
Disease Models, Animal
DNA Damage - drug effects
Endometrial Neoplasms
Female
Humans
Mice
Models, Biological
Research Paper
Xenograft Model Antitumor Assays
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Summary:Endometrial cancer is the most common cancer in women, typically with onset after menopause. Isoliquiritigenin (ISL), a licorice flavonoid, was previously shown to have anti-oxidant, anti-inflammatory, and tumor suppression effects. In this study, we investigated the anti-tumor effect of ISL on human endometrial cancer both in vitro and in vivo. We used telomerase-immortalized human endometrial stromal cells (T-HESCs) and human endometrial cancer cell lines (Ishikawa, HEC-1A, and RL95-2 cells) as targets. The effects of ISL on cell proliferation, cell cycle regulation, and apoptosis or autophagy-related protein expression were examined. In addition, we conducted in vivo experiments to confirm the inhibitory effects of ISL on cancer cells. ISL significantly inhibited the viability of cancer cells in a dose- and time-dependent manner but with little toxicity on normal cells. In addition, flow cytometry analysis indicated that ISL induced sub-G1 or G2/M phase arrest. ISL treatment activated the extracellular signal regulated kinase signaling pathway to enhance the protein expression of caspase-7/LC3BII associated with apoptosis/autophagy. Furthermore, ISL suppressed xenograft tumor growth in vivo. Taken together, these findings suggest that ISL may induce apoptosis, autophagy, and cell growth inhibition, indicating its potential as a therapeutic agent for human endometrial cancer.
ISSN:1949-2553
1949-2553
DOI:10.18632/oncotarget.12369