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This article is part of the supplement: Abstracts of the 16th International Charles Heidelberger Symposium on Cancer Research

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Cr(VI)-induced malignant transformation of a bronchial epithelial cell line association with altered mitochondria and bioenergetic phenotypes

Ana Sampaio14*, Luís Mendes14, Ana C Gonçalves2, A Margarida Abrantes24, Ana B Sarmento24, Filomena Botelho24, Paulo Oliveira3, Vilma Sardão3, Rui Carvalho1, Ana M Urbano145 and M Carmen Alpoim134

Author Affiliations

1 Departamento de Ciências da Vida, FCTUC, Universidade de Coimbra, Coimbra, Portugal

2 Faculdade of Medicina, Universidade de Coimbra, Coimbra, Portugal

3 Centro de Neurociências e Biologia Celular, Coimbra, Portugal

4 Centro de Investigação em Meio Ambiente, Genética, e Oncobiologia (CIMAGO), Faculdade of Medicina, Universidade de Coimbra, Coimbra, Portugal

5 Unidade de Química-Física Molecular, FCTUC, Universidade de Coimbra, Coimbra, Portugal

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BMC Proceedings 2010, 4(Suppl 2):P17  doi:10.1186/1753-6561-4-S2-P17

The electronic version of this article is the complete one and can be found online at:

Published:24 September 2010

© 2010 Sampaio et al; licensee BioMed Central Ltd.

Poster presentation

Mitochondria play important roles in cellular energy metabolism, free radical generation, cell signaling and apoptosis. Defects in mitochondrial function have long been suspected to contribute to the development and progression of cancer. Warburg's pioneering work hypothesized that a key event in carcinogenesis involved changes in metabolism, with malignant cells satisfying their energy needs by producing a large portion of their ATP through glycolytic mechanisms, rather than through oxidative phosphorylation. Certain malignant cells have also been reported to have alterations in mitochondrial content as compared to normal cells of the same tissue. In lung fibroblasts, taken from a lung epidermoid carcinoma, low mitochondria content was associated with decreased oxidative phosphorylation and increased glycolysis. Also, recently, it was revealed that, in vitro Cr(VI)-induced malignant transformation of BEAS-2B cells was associated with the inhibition of mitochondrial pathway of apoptosis.

Aiming to establish whether the malignant transformation of bronchial epithelial cells was paralleled by changes in cellular bioenergetic and mitochondrial phenotypes, we evaluated the energy metabolism, the mitochondria membrane potential and the mitochondria content in a normal bronchial epithelial cell line and in its malignant derivatives. To this end, the mitochondria membrane potential was evaluated by flow cytometry using the JC-1 fluorescent probe. Fluorescence microscopy was used to evaluate the mitocondria morphology and number, and 1H spectroscopy was used to assess the cell’s bioenergetic phenotype. Our results revealed that the more malignant phenotypes correlate with increased mitochondria biogenesis, decreased membrane potential and altered bioenergetic phenotype.


This work was supported by CIMAGO (Grant CIMAGO 16/06).