Please use this identifier to cite or link to this item: https://doi.org/10.3390/molecules22081272
Title: Artesunate activates the intrinsic apoptosis of HCT116 cells through the suppression of fatty acid synthesis and the NF-?B pathway
Authors: Chen, X
Wong, Y.K
Lim, T.K 
Lim, W.H
Lin, Q 
Wang, J 
Hua, Z
Keywords: artemisinin derivative
artesunate
fatty acid
immunoglobulin enhancer binding protein
reactive oxygen metabolite
apoptosis
biological model
biosynthesis
cell proliferation
cell survival
dose response
drug effects
HCT 116 cell line
human
metabolism
mitochondrion
procedures
proteomics
signal transduction
Apoptosis
Artemisinins
Biosynthetic Pathways
Cell Proliferation
Cell Survival
Dose-Response Relationship, Drug
Fatty Acids
HCT116 Cells
Humans
Mitochondria
Models, Biological
NF-kappa B
Proteomics
Reactive Oxygen Species
Signal Transduction
Issue Date: 2017
Publisher: MDPI AG
Citation: Chen, X, Wong, Y.K, Lim, T.K, Lim, W.H, Lin, Q, Wang, J, Hua, Z (2017). Artesunate activates the intrinsic apoptosis of HCT116 cells through the suppression of fatty acid synthesis and the NF-?B pathway. Molecules 22 (8) : 1272. ScholarBank@NUS Repository. https://doi.org/10.3390/molecules22081272
Abstract: The artemisinin compounds, which are well-known for their potent therapeutic antimalarial activity, possess in vivo and in vitro antitumor effects. Although the anticancer effect of artemisinin compounds has been extensively reported, the precise mechanisms underlying its cytotoxicity remain under intensive study. In the present study, a high-throughput quantitative proteomics approach was applied to identify differentially expressed proteins of HCT116 colorectal cancer cell line with artesunate (ART) treatment. Through Ingenuity Pathway Analysis, we discovered that the top-ranked ART-regulated biological pathways are abrogation of fatty acid biosynthetic pathway and mitochondrial dysfunction. Subsequent assays showed that ART inhibits HCT116 cell proliferation through suppressing the fatty acid biosynthetic pathway and activating the mitochondrial apoptosis pathway. In addition, ART also regulates several proteins that are involved in NF-?B pathway, and our subsequent assays showed that ART suppresses the NF-?B pathway. These proteomic findings will contribute to improving our understanding of the underlying molecular mechanisms of ART for its therapeutic cytotoxic effect towards cancer cells. © 2017 by the authors.
Source Title: Molecules
URI: https://scholarbank.nus.edu.sg/handle/10635/175156
ISSN: 1420-3049
DOI: 10.3390/molecules22081272
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