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J Proteome Res. 2018 Apr 20;:
Authors: Xing YX, Li MH, Tao L, Ruan LY, Hong W, Chen C, Zhao WL, Xu H, Chen JF, Wang JS
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 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.
PMID: 29676152 [PubMed - as supplied by publisher]
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Anti-cancer effects of emodin on HepG2 cells as revealed by 1H-NMR based metabolic profiling.
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