期刊
ONCOTARGETS AND THERAPY
卷 14, 期 -, 页码 5131-5144出版社
DOVE MEDICAL PRESS LTD
DOI: 10.2147/OTT.S322852
关键词
18 beta-glycyrrhetinic acid; lung cancer; apoptosis; cell cycle arrest; ROS; cell migration
资金
- central government supports local college reform and development fund talent training projects [2020GSP16]
- Heilongjiang Farms & Land Reclamation Administration Support Project for Key Scientific Research [HKKYZD190705]
- Heilongjiang Bayi Agricultural University Support Program for San Zong [TDJH201905]
- Heilongjiang Touyan Innovation Team Program [2019HTY078]
- Project for Heilongjiang Bayi Agricultural University [XDB202012]
- Heilongjiang Province College Student Innovation and Entrepreneurship Training Program Project [202010223004, 202010223001]
The study demonstrated that 18 beta-glycyrrhetinic acid induces apoptosis and G2/M cell cycle arrest, as well as inhibits migration in A549 lung cancer cells through the activation of the ROS/MAPK/STAT3/NF-kappa B signaling pathways.
Background: 18 beta-glycyrrhetinic acid (18 beta-Gly), which is extracted from licorice root, has various pharmacological properties; however, its anti-cancer effects on lung cancer cells have not been fully established. Purpose: In this study, we investigated the underlying molecular mechanisms of 18 beta-Gly. Results: Our results showed that 18 beta-Gly had significant cytotoxic effects and no apparent side effects. 18 beta-Gly induced mitochondria-dependent apoptosis of A549 lung cancer cells. In addition, after treatment with 18 beta-Gly, intracellular reactive oxygen species (ROS) levels were significantly increased, and G2/M cell cycle arrest and inhibition of cell migration were induced via the mitogen-activated protein kinase (MAPK)/signal transducer and activator of transcription 3 (STAT3)/nuclear factor kappa (NF-kappa B) signaling pathways. After pretreatment with the ROS scavenger N-acetyl-L-cysteine or MAPK inhibitors, the expression levels of phosphorylated p38 (p-p38), phosphorylated c-Jun N-terminal kinase, inhibitor of nuclear factor kappa B, cleaved caspase-3 (cle-cas-3), cleaved poly (ADP ribose) polymerase (cle-PARP), p-p53, p27, p21, and E-cadherin were decreased; and levels of phosphorylated dependent kinase 1/2 (CDK1/2), N-cadherin, vimentin, and snail homolog 1 (SNAI 1) were increased. In addition, the percentage of cells in the G2/M phase was decreased, and inhibition of migration was reduced. Conclusion: In summary, 18 beta-Gly induced apoptosis and G2/M cell cycle arrest and inhibited migration via the ROS/MAPK/STAT3/NF-kappa B signaling pathways in A549 lung cancer cells. Therefore, 18 beta-Gly is a novel promising candidate for the treatment of lung cancer.
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