ArticleBMC systems biology2010
Edelfosine-induced metabolic changes in cancer cells that precede the overproduction of reactive oxygen species and apoptosis.
Article in BMC systems biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 28 citations in OpenAlex.
- Bayesian kinetic modeling for tracer-based metabolomic data.BMC bioinformatics · 2023Article
- The landscape of tiered regulation of breast cancer cell metabolism.Scientific reports · 2019Article
- PhenoMeNal: processing and analysis of metabolomics data in the cloud.GigaScience · 2019Article
- MIDcor, an R-program for deciphering mass interferences in mass spectra of metabolites enriched in stable isotopes.BMC bioinformatics · 2017Article
- HepatoDyn: A Dynamic Model of Hepatocyte Metabolism That Integrates 13C Isotopomer Data.PLoS computational biology · 2016Article
- Applications of NMR spectroscopy to systems biochemistry.Progress in nuclear magnetic resonance spectroscopy · 2016Review
- (13)C metabolic flux analysis shows that resistin impairs the metabolic response to insulin in L6E9 myotubes.BMC systems biology · 2014Article
- Stable isotope-resolved metabolomics and applications for drug development.Pharmacology & therapeutics · 2012Review
- Compartmentation of glycogen metabolism revealed from 13C isotopologue distributions.BMC systems biology · 2011Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundMetabolic flux profiling based on the analysis of distribution of stable isotope tracer in metabolites is an important method widely used in cancer research to understand the regulation of cell metabolism and elaborate new therapeutic strategies. Recently, we developed software Isodyn, which extends the methodology of kinetic modeling to the analysis of isotopic isomer distribution for the evaluation of cellular metabolic flux profile under relevant conditions. This tool can be applied to reveal the metabolic effect of proapoptotic drug edelfosine in leukemia Jurkat cell line, uncovering the mechanisms of induction of apoptosis in cancer cells.
resultsThe study of 13C distribution of Jukat cells exposed to low edelfosine concentration, which induces apoptosis in ≤5% of cells, revealed metabolic changes previous to the development of apoptotic program. Specifically, it was found that low dose of edelfosine stimulates the TCA cycle. These metabolic perturbations were coupled with an increase of nucleic acid synthesis de novo, which indicates acceleration of biosynthetic and reparative processes. The further increase of the TCA cycle fluxes, when higher doses of drug applied, eventually enhance reactive oxygen species (ROS) production and trigger apoptotic program.
conclusionThe application of Isodyn to the analysis of mechanism of edelfosine-induced apoptosis revealed primary drug-induced metabolic changes, which are important for the subsequent initiation of apoptotic program. Initiation of such metabolic changes could be exploited in anticancer therapy.
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Registered trials
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