Liquiritigenin Induces Tumor Cell Death through Mitogen-Activated Protein Kinase- MPAKs- Mediated Pathway in Hepatocellular Carcinoma CellsReport as inadecuate




Liquiritigenin Induces Tumor Cell Death through Mitogen-Activated Protein Kinase- MPAKs- Mediated Pathway in Hepatocellular Carcinoma Cells - Download this document for free, or read online. Document in PDF available to download.

BioMed Research International - Volume 2014 2014, Article ID 965316, 11 pages -

Research Article

College of Life Science, Jilin University, Changchun, Jilin 130012, China

The State Engineering Laboratory of AIDS Vaccine, Jilin University, Changchun 130012, China

Received 9 December 2013; Revised 24 January 2014; Accepted 4 February 2014; Published 11 March 2014

Academic Editor: Thomas Griffith

Copyright © 2014 Di Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Liquiritigenin LQ, separated from Glycyrrhiza radix, possesses anti-inflammatory, antihyperlipidemic, and antiallergic effects. Our present study aims to investigate the antihepatocellular carcinoma effects of LQ both in cell and animal models. LQ strikingly reduced cell viability, enhanced apoptotic rate, induced lactate dehydrogenase over-release, and increased intracellular reactive oxygen species ROS level and caspase 3 activity in both PLC-PRL-5 and HepG2 cells. The expression of cleaved PARP, the hall-marker of apoptosis, was enhanced by LQ. LQ treatment resulted in a reduction of the expressions of B-cell lymphoma 2 Bcl-2 and B-cell lymphoma-extra large Bcl-xL, and an increase of the phosphorylation of c-Jun N-terminal kinases JNK and P38. LQ-mediated cell viability reduction, mitochondrial dysfunction, apoptosis related protein abnormal expressions, and JNK and P38 activation were partially abolished by N-Acetyl-L-cysteine a ROS inhibitor pretreatment. Moreover, LQ suppressed the activation of extracellular signaling-regulated kinase ERKs and reduced the translocation of phosphor-ERKs from cytoplasm to nucleus. This antitumor activity was further confirmed in PLC-PRL-5-xenografted mice model. All these data indicate that the antihepatocellular carcinoma effects of LQ are related to its modulation of the activations of mitogen-activated protein kinase MAPKs. The study provides experimental evidence supporting LQ as a potential therapeutic agent for hepatocellular carcinoma treatment.





Author: Di Wang, Jiahui Lu, Yan Liu, Qingfan Meng, Jing Xie, Zhenzuo Wang, and Lesheng Teng

Source: https://www.hindawi.com/



DOWNLOAD PDF




Related documents