ArticleMolecular systems biology2011
Glucose metabolism determines resistance of cancer cells to bioenergetic crisis after cytochrome-c release.
Article in Molecular systems biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- Mitochondria affect antibacterial immunity in cross talk with innate immune response molecules coded by genes of nuclear origin.Frontiers in immunology · 2026Article
- Integrating simulated and experimental data to identify mitochondrial bioenergetic defects in Parkinson's Disease models.PloS one · 2026Article
- Understanding metabolic plasticity at single cell resolution.Essays in biochemistry · 2024Review
- Exploring metabolism in scleroderma reveals opportunities for pharmacological intervention for therapy in fibrosis.Frontiers in immunology · 2022Article
- Two-level modeling approach to identify the regulatory dynamics capturing drug response heterogeneity in single-cells.Scientific reports · 2021Article
- Reduction in mitochondrial oxidative stress mediates hypoxia-induced resistance to cisplatin in human transitional cell carcinoma cells.Neoplasia (New York, N.Y.) · 2021Article
- Mitochondrial DNA in inflammation and immunity.EMBO reports · 2020Review
- Systems biology identifies preserved integrity but impaired metabolism of mitochondria due to a glycolytic defect in Alzheimer's disease neurons.Aging cell · 2019Article
- High glycolytic activity of tumor cells leads to underestimation of electron transport system capacity when mitochondrial ATP synthase is inhibited.Scientific reports · 2018Article
- Mitochondrial inner membrane permeabilisation enables mtDNA release during apoptosis.The EMBO journal · 2018Article
- Influence of Pulsed Electric Fields and Mitochondria-Cytoskeleton Interactions on Cell Respiration.Biophysical journal · 2018Article
- Article
- Hexokinase 2 and nuclear factor erythroid 2-related factor 2 transcriptionally coactivate xanthine oxidoreductase expression in stressed glioma cells.The Journal of biological chemistry · 2018Article
- Single-cell time-lapse imaging of intracellular OCell death & disease · 2017Article
- Doxorubicin-induced chronic dilated cardiomyopathy-the apoptosis hypothesis revisited.Journal of molecular medicine (Berlin, Germany) · 2017Review
- Hypoxia and classical activation limits Mycobacterium tuberculosis survival by Akt-dependent glycolytic shift in macrophages.Cell death discovery · 2016Article
- PARP14 promotes the Warburg effect in hepatocellular carcinoma by inhibiting JNK1-dependent PKM2 phosphorylation and activation.Nature communications · 2015Article
- Induction of human chronic myeloid leukemia K562 cell apoptosis by virosecurinine and its molecular mechanism.Molecular medicine reports · 2014Article
- Single-cell imaging tools for brain energy metabolism: a review.Neurophotonics · 2014Article
- From computational modelling of the intrinsic apoptosis pathway to a systems-based analysis of chemotherapy resistance: achievements, perspectives and challenges in systems medicine.Cell death & disease · 2014Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many anticancer drugs activate caspases via the mitochondrial apoptosis pathway. Activation of this pathway triggers a concomitant bioenergetic crisis caused by the release of cytochrome-c (cyt-c). Cancer cells are able to evade these processes by altering metabolic and caspase activation pathways. In this study, we provide the first integrated system study of mitochondrial bioenergetics and apoptosis signalling and examine the role of mitochondrial cyt-c release in these events. In accordance with single-cell experiments, our model showed that loss of cyt-c decreased mitochondrial respiration by 95% and depolarised mitochondrial membrane potential ΔΨ(m) from -142 to -88 mV, with active caspase-3 potentiating this decrease. ATP synthase was reversed under such conditions, consuming ATP and stabilising ΔΨ(m). However, the direction and level of ATP synthase activity showed significant heterogeneity in individual cancer cells, which the model explained by variations in (i) accessible cyt-c after release and (ii) the cell's glycolytic capacity. Our results provide a quantitative and mechanistic explanation for the protective role of enhanced glucose utilisation for cancer cells to avert the otherwise lethal bioenergetic crisis associated with apoptosis initiation.
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