Difference between revisions of "El-Bacha MiP2010"
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{{Publication | {{Publication | ||
|title=Amoedo ND, Figueiredo MR, Pezutto P, Lourenco MVC, Madeiro da Costa RF, Oliveira MFO, Galina A, Rumjanek FD, El-Bacha T (2010) Metabolic reprogramming of lung cancer cell induced by sodium butyrate: studies on mitochondrial physiology and bioenergetics. Mitochondr. Physiol. Network 15.6: 81. | |title=Amoedo ND, Figueiredo MR, Pezutto P, Lourenco MVC, Madeiro da Costa RF, Oliveira MFO, Galina A, Rumjanek FD, El-Bacha T (2010) Metabolic reprogramming of lung cancer cell induced by sodium butyrate: studies on mitochondrial physiology and bioenergetics. Mitochondr. Physiol. Network 15.6: 81. | ||
|info=[http://www.mitophysiology.org/index.php?mip2010-session4 Abstracts Session 4] | |||
|authors=Amoedo ND, Figueiredo MR, Pezutto P, Lourenco MVC, Madeiro da Costa RF, Oliveira MFO, Galina A, Rumjanek FD, El-Bacha T | |authors=Amoedo ND, Figueiredo MR, Pezutto P, Lourenco MVC, Madeiro da Costa RF, Oliveira MFO, Galina A, Rumjanek FD, El-Bacha T | ||
|year=2010 | |year=2010 | ||
|mipnetlab=BR RioDeJaneiro GalinaA | |mipnetlab=BR RioDeJaneiro GalinaA | ||
|abstract=Tumor cells are characterized by accelerated growth usually accompanied by up-regulated pathways that ultimately increase the rate of ATP production. These cells can suffer metabolic reprogramming, resulting in distinct bioenergetic phenotypes, generally enhancing glycolysis channelled to lactate production [1]. It has been highlighted that maintenance of energy homeostasis (both oxidative and glycolytic metabolism) is essential for tumor development control [2]. In this context we have investigated whether sodium butyrate (NaB), a histone deacetylase inhibitor, alters the energy metabolism in lung cancer cells (H460) and if these effects are related to differentiation, growth arrest and apoptosis observed in these cells exposed to 10 mM NaB during 24 hours. We have shown that in this experimental condition, cells display reduced glycolytic flux indicated by lactate production. Results with [[high-resolution respirometry]] show increased oxidative metabolism leading to increased rates of oxygen consumption coupled to ATP synthesis. Mitochondria morphology, characterized by electron microscopy, showed increased size in the treated cells. These results can be associated to mitochondrial fusion because we have detected an increase in mitofusin mRNA. These alterations on the energetic metabolism after treatment with NaB suggest that there is an increase in mitochondrial function and enhanced oxidative metabolism. | |abstract=Tumor cells are characterized by accelerated growth usually accompanied by up-regulated pathways that ultimately increase the rate of ATP production. These cells can suffer metabolic reprogramming, resulting in distinct bioenergetic phenotypes, generally enhancing glycolysis channelled to lactate production [1]. It has been highlighted that maintenance of energy homeostasis (both oxidative and glycolytic metabolism) is essential for tumor development control [2]. In this context we have investigated whether sodium butyrate (NaB), a histone deacetylase inhibitor, alters the energy metabolism in lung cancer cells (H460) and if these effects are related to differentiation, growth arrest and apoptosis observed in these cells exposed to 10 mM NaB during 24 hours. We have shown that in this experimental condition, cells display reduced glycolytic flux indicated by lactate production. Results with [[high-resolution respirometry]] show increased oxidative metabolism leading to increased rates of oxygen consumption coupled to ATP synthesis. Mitochondria morphology, characterized by electron microscopy, showed increased size in the treated cells. These results can be associated to mitochondrial fusion because we have detected an increase in mitofusin mRNA. These alterations on the energetic metabolism after treatment with NaB suggest that there is an increase in mitochondrial function and enhanced oxidative metabolism. | ||
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2. Xu WS, Parmigiani RB, Marks PA (2007) Histone deacetylase inhibitors: molecular mechanisms of action. Oncogene 26: 5541-5552. | 2. Xu WS, Parmigiani RB, Marks PA (2007) Histone deacetylase inhibitors: molecular mechanisms of action. Oncogene 26: 5541-5552. | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
Revision as of 18:48, 9 March 2011
| Amoedo ND, Figueiredo MR, Pezutto P, Lourenco MVC, Madeiro da Costa RF, Oliveira MFO, Galina A, Rumjanek FD, El-Bacha T (2010) Metabolic reprogramming of lung cancer cell induced by sodium butyrate: studies on mitochondrial physiology and bioenergetics. Mitochondr. Physiol. Network 15.6: 81. |
Amoedo ND, Figueiredo MR, Pezutto P, Lourenco MVC, Madeiro da Costa RF, Oliveira MFO, Galina A, Rumjanek FD, El-Bacha T (2010)
Abstract: Tumor cells are characterized by accelerated growth usually accompanied by up-regulated pathways that ultimately increase the rate of ATP production. These cells can suffer metabolic reprogramming, resulting in distinct bioenergetic phenotypes, generally enhancing glycolysis channelled to lactate production [1]. It has been highlighted that maintenance of energy homeostasis (both oxidative and glycolytic metabolism) is essential for tumor development control [2]. In this context we have investigated whether sodium butyrate (NaB), a histone deacetylase inhibitor, alters the energy metabolism in lung cancer cells (H460) and if these effects are related to differentiation, growth arrest and apoptosis observed in these cells exposed to 10 mM NaB during 24 hours. We have shown that in this experimental condition, cells display reduced glycolytic flux indicated by lactate production. Results with high-resolution respirometry show increased oxidative metabolism leading to increased rates of oxygen consumption coupled to ATP synthesis. Mitochondria morphology, characterized by electron microscopy, showed increased size in the treated cells. These results can be associated to mitochondrial fusion because we have detected an increase in mitofusin mRNA. These alterations on the energetic metabolism after treatment with NaB suggest that there is an increase in mitochondrial function and enhanced oxidative metabolism.
1. Kroemer G, Pouyssegur J (2008) Tumor cell metabolism: cancer's Achilles' heel. Cancer Cell 13: 472-482.
2. Xu WS, Parmigiani RB, Marks PA (2007) Histone deacetylase inhibitors: molecular mechanisms of action. Oncogene 26: 5541-5552.
• O2k-Network Lab: BR RioDeJaneiro GalinaA
Labels:
Stress:Cancer; Apoptosis; Cytochrome c"Cancer; Apoptosis; Cytochrome c" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property.
Preparation: Intact Cell; Cultured; Primary"Intact Cell; Cultured; Primary" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.
Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.
HRR: Oxygraph-2k
Lung
