Rodrigues 2012 Abstract IOC72

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Rodrigues MF, Amoedo ND, Rumjanek FD (2012) Studies of bioenergetics alterations in breast cancer lines induced by sodium butyrate. Mitochondr Physiol Network 17.13.

Link: IOC72 Open Access

Rodrigues MF, Amoedo ND, Rumjanek FD (2012)

Event: IOC72

Figueiredo Mariana

Tumor cells are characterized by a different bioenergetic phenotype compared to normal cells. This phenotype can change with the microenviroment, tumor progression and tumorigenicity. Many cancer cells display enhanced glycolysis even if the oxygen tension is normal (aerobic glycolysis or Warburg effect). Contrary to what was believed initially mitochondrial function can be important for tumor development [1]. Results in the literature show various effects caused by histone deacetylase inhibitors (HDACis), which induce accumulation of acetylated substrates, generating cell cycle arrest, differentiation and cell death [2]. However, little is known about HDACis effects in the energy metabolism modulation. Recent studies have shown that HDACis are able to modulate the glycolytic metabolism and mitochondrial function from highly glycolytic lung tumor cells [3]. In this context we have investigated how sodium butyrate (NaB), a histone deacetylase inhibitor, alters the energy metabolism in breast tumor cell lines with different stages of tumorigenicity. We observed that NaB treatment induced an attenuation of glycolysis, reflected by a decrease in lactate release in MCF-7 and T47D lines. Furthermore, the treatment induced an increase in ROUTINE, LEAK and ET-pathway respiration in T47D, while no change was observed in MCF-7. Interestingly, we observed an increase in ROX respiration of MDA-MB-231, suggesting that NaB can induce the activity of other oxidases. Taken together, these results showed that cells in different stages of tumorigenic progression react differently to NaB which highlight the fact that they exhibit different metabolic profiles, especially in what concerns their energy status.

[1] Smolkova K, Plecita-Hlavata L, Bellance N, Benard G, Rossignol R, Jezek P (2011) Waves of gene regulation suppress and then restore oxidative phosphorylation in cancer cells. Int J Biochem Cell Biol 43:950-968

[2] Schrump DS (2009) Cytotoxicity mediated by histone deacetylase inhibitors in cancer cells: mechanisms and potential clinical implications Clin Cancer Res 15: 3947-3957 Open Access

[3] Amoedo ND, Rodrigues MF, Pezzuto P, Galina A, da Costa RM, de Almeida FC, El-Bacha T, Rumjanek FD (2011) Energy metabolism in h460 lung cancer cells: effects of histone deacetylase inhibitors. PLoS One 6: e22264

Keywords: HDACis, Sodium Butyrate, Breast Cancer Cells, Metabolism

O2k-Network Lab: BR Rio de Janeiro Rumjanek FD


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Coupling state: LEAK, ROUTINE, ET 

HRR: Oxygraph-2k 




Affiliations and author contributions

Rodrigues MF (1), Amoedo ND (1), Rumjanek FD (1)

(1) Instituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil; Email: mfrodrigues@bioqmed.ufrj.br


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