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Open AccessArticle

Anti-Proliferative and Pro-Apoptotic Effects of Licochalcone A through ROS-Mediated Cell Cycle Arrest and Apoptosis in Human Bladder Cancer Cells

1
Anti-Aging Research Center, Dong-eui University, Busan 47227, Korea
2
Department of Biochemistry, Dong-eui University College of Korean Medicine, Busan 47227, Korea
3
Department of Parasitology and Genetics, Kosin University College of Medicine, Busan 49267, Korea
4
Department of Molecular Biology, College of Natural Sciences, Pusan National University, Busan 46241, Korea
5
Department of Molecular Biology, College of Natural Sciences, Dong-eui University, Busan 47340, Korea
6
Department of Marine Life Sciences, School of Marine Biomedical Sciences, Jeju National University, Jeju 63243, Korea
7
Department of Food and Nutrition, Chung-Ang University, Anseong 17546, Korea
8
Department of Urology, College of Medicine, Chungbuk National University, Chungbuk 8644, Korea
9
Department of Cell Biology, Catholic University of Daegu School of Medicine, Daegu 42472, Korea
*
Authors to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2019, 20(15), 3820; https://doi.org/10.3390/ijms20153820
Received: 13 July 2019 / Revised: 2 August 2019 / Accepted: 2 August 2019 / Published: 5 August 2019
(This article belongs to the Special Issue Bioactive Phytochemicals for Cancer Prevention and Treatment)
Licochalcone A (LCA) is a chalcone that is predominantly found in the root of Glycyrrhiza species, which is widely used as an herbal medicine. Although previous studies have reported that LCA has a wide range of pharmacological effects, evidence for the underlying molecular mechanism of its anti-cancer efficacy is still lacking. In this study, we investigated the anti-proliferative effect of LCA on human bladder cancer cells, and found that LCA induced cell cycle arrest at G2/M phase and apoptotic cell death. Our data showed that LCA inhibited the expression of cyclin A, cyclin B1, and Wee1, but increased the expression of cyclin-dependent kinase (Cdk) inhibitor p21WAF1/CIP1, and increased p21 was bound to Cdc2 and Cdk2. LCA activated caspase-8 and -9, which are involved in the initiation of extrinsic and intrinsic apoptosis pathways, respectively, and also increased caspase-3 activity, a typical effect caspase, subsequently leading to poly (ADP-ribose) polymerase cleavage. Additionally, LCA increased the Bax/Bcl-2 ratio, and reduced the integrity of mitochondria, which contributed to the discharge of cytochrome c from the mitochondria to the cytoplasm. Moreover, LCA enhanced the intracellular levels of reactive oxygen species (ROS); however, the interruption of ROS generation using ROS scavenger led to escape from LCA-mediated G2/M arrest and apoptosis. Collectively, the present data indicate that LCA can inhibit the proliferation of human bladder cancer cells by inducing ROS-dependent G2/M phase arrest and apoptosis. View Full-Text
Keywords: Licochalcone A; bladder cancer; G2/M arrest; apoptosis; ROS Licochalcone A; bladder cancer; G2/M arrest; apoptosis; ROS
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Hong, S.H.; Cha, H.-J.; Hwang-Bo, H.; Kim, M.Y.; Kim, S.Y.; Ji, S.Y.; Cheong, J.; Park, C.; Lee, H.; Kim, G.-Y.; Moon, S.-K.; Yun, S.J.; Chang, Y.-C.; Kim, W.-J.; Choi, Y.H. Anti-Proliferative and Pro-Apoptotic Effects of Licochalcone A through ROS-Mediated Cell Cycle Arrest and Apoptosis in Human Bladder Cancer Cells. Int. J. Mol. Sci. 2019, 20, 3820.

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