Liquiritin inhibits proliferation and induces apoptosis in HepG2 hepatocellular carcinoma cells via the ROS-mediated MAP
- PDF / 7,409,857 Bytes
- 13 Pages / 595.276 x 790.866 pts Page_size
- 80 Downloads / 203 Views
ORIGINAL ARTICLE
Liquiritin inhibits proliferation and induces apoptosis in HepG2 hepatocellular carcinoma cells via the ROS-mediated MAPK/AKT/NF-κB signaling pathway Jia-Ru Wang 1 & Tian-Zhu Li 2 & Cheng Wang 3 & Shu-Mei Li 4 & Ying-Hua Luo 5 & Xian-Ji Piao 6 & Yu-Chao Feng 7 & Yi Zhang 1 & Wan-Ting Xu 1 & Yu Zhang 1 & Tong Zhang 1 & Shi-Nong Wang 1 & Hui Xue 1 & Hong-Xing Wang 1 & Long-Kui Cao 7,8 & Cheng-Hao Jin 1,7,8 Received: 21 July 2019 / Accepted: 1 November 2019 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Liquiritin (LIQ), a major constituent of Glycyrrhiza Radix, exhibits various pharmacological activities. In this study, to explore the potential anti-cancer effects and its underlying molecular mechanisms of LIQ in hepatocellular carcinoma (HCC) cells. LIQ significantly decreased viability and induced apoptosis in HepG2 cells by decreasing mitochondrial membrane potential and regulating Bcl-2 family proteins, cytochrome c, cle-caspase-3, and cle-PARP. The cell cycle analysis and western blot analysis revealed that LIQ induced G2/M phase arrest through increased expression of p21 and decreased levels of p27, cyclin B, and CDK1/2. The flow cytometry and western blot analysis also suggested that LIQ promoted the accumulation of ROS in HepG2 cells and up-regulated the phosphorylation expression levels of p38 kinase, c-Jun N-terminal kinase (JNK), and inhibitor of NF-κB (IκB-α); the phosphorylation levels of extracellular signal-regulated kinase (ERK), protein kinase B (AKT), signal transducer activator of transcription 3 (STAT3), and nuclear factor kappa B (NF-κB) were down-regulated. However, these effects were reversed by N-acetyl-L-cysteine (NAC), MAPK, and AKT inhibitors. The findings demonstrated that LIQ induced cell cycle arrest and apoptosis via the ROS-mediated MAPK/AKT/NF-κB signaling pathway in HepG2 cells, and the LIQ may serve as a potential therapeutic agent for the treatment of human HCC. Keywords Liquiritin . Human hepatocellular carcinoma cells . Apoptosis . Cell cycle arrest . Reactive oxygen species
Jia-Ru Wang, Tian-Zhu Li, and Cheng Wang contributed equally to this work. Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00210-019-01763-7) contains supplementary material, which is available to authorized users. * Cheng-Hao Jin [email protected] * Long-Kui Cao [email protected] 1
Department of Biochemistry and Molecular Biology, College of Life Science & Technology, Heilongjiang Bayi Agricultural University, Daqing 163319, China
2
Molecular Medicine Research Center, School of Basic Medical Science, Chifeng University, Chifeng 024000, China
3
Pharmacy Department, Daqing Oilfield General Hospital, Daqing 163001, China
4
Hemodialysis Center, Daqing Oilfield General Hospital, Daqing 163001, China
5
Department of Grass Science, College of Animal Science & Veterinary Medicine, Heilongjiang Bayi Agricultural University, Daqing 163319, China
6
Department of Gynaecology and Obstetrics, the Fifth Affiliated
Data Loading...
