| Literature DB >> 29676152 |
Yue-Xiao Xing1, Ming-Hui Li1, Liang Tao1, Ling-Yu Ruan1, Wei Hong1, Cheng Chen1, Wen-Long Zhao1, Han Xu1, Jian-Feng Chen1, Jun-Song Wang1.
Abstract
Hepatic carcinoma is one of the most common cancers in the world, with a high incidence. Emodin is an anthraquinone derived from Polygonum multiflorum Thunb, possessing anti-cancer activity. The purpose of this study is to investigate the anti-cancer effect of different dosages of emodin on HepG2 cells using a 1H NMR based metabolic approach complemented with qRT-PCR and flow cytometry to identify potential markers and discover the targets to explore the underlying mechanism. Emodin can dose-dependently inhibit the growth of HepG2 cells, perturb cell cycle progression, down-regulate the expression of genes and proteins related to glycolysis, and trigger intracellular ROS generation. Orthogonal signal correction partial least-squares discriminant analysis (OSC-PLS-DA) and correlation network analysis of the 1H NMR data showed significant changes in many endogenous metabolites after emodin exposure concerning oxidative stress and disturbances in amino acid and energy metabolism. These findings are helpful to understand the anti-cancer mechanism of emodin and provide a theoretical basis for its future application and development.Entities:
Keywords: HepG2; ROS; anti-cancer; emodin; energy metabolism; glycolysis; metabolomics
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Year: 2018 PMID: 29676152 DOI: 10.1021/acs.jproteome.8b00029
Source DB: PubMed Journal: J Proteome Res ISSN: 1535-3893 Impact factor: 4.466