Amoedo 2010 Abstract MiP2010

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Amoêdo ND, Rodrigues MF, Pezutto P, Lourenço MVC, Madeiro da Costa RF, Oliveira MF, 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 15.06.

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Amoedo ND, Rodrigues MF, Pezutto P, Lourenco MVC, Madeiro da Costa RF, Oliveira MF, Galina A, Rumjanek FD, El-Bacha T (2010)

Event: MiP2010

Tumour 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 tumour 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 10mM 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 Rio de Janeiro Rumjanek FD, BR Rio de Janeiro Galina A, BR Rio de Janeiro Oliveira MF


Labels: MiParea: Respiration, Pharmacology;toxicology  Pathology: Cancer 

Organism: Human  Tissue;cell: Endothelial;epithelial;mesothelial cell, Fibroblast  Preparation: Intact cells  Enzyme: Complex I, Complex II;succinate dehydrogenase  Regulation: Aerobic glycolysis, ADP, Substrate, Amino acid  Coupling state: OXPHOS, ET 

HRR: Oxygraph-2k