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

Open Access Poster presentation

Polyaromatic hydrocarbons accentuate malignant phenotype of the PC3 prostate cancer cell line

Mariana O Freitas123*, José Oliveira1, Ana M Fernandes1, Maria I Coutinho1, Vera Alves4, Anabela Mota-Pinto12 and Ana B Sarmento-Ribeiro235

Author Affiliations

1 General Pathology Institute, Faculty of Medicine, University of Coimbra, Coimbra, Portugal

2 Center for Investigation in Environment, Genetics and Oncobiology (CIMAGO), Coimbra, Portugal

3 Center of Neurosciences and Cell Biology (CNC), University of Coimbra, Coimbra, Portugal

4 Immunology Institute, Faculty of Medicine, University of Coimbra, Coimbra, Portugal

5 Biochemistry Institute, Faculty of Medicine, University of Coimbra, Coimbra, Portugal

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BMC Proceedings 2010, 4(Suppl 2):P26  doi:10.1186/1753-6561-4-S2-P26

The electronic version of this article is the complete one and can be found online at: http://www.biomedcentral.com/1753-6561/4/S2/P26


Published:24 September 2010

© 2010 Freitas et al; licensee BioMed Central Ltd.

Poster presentation

Prostate cancer risk factors are mainly associated to an increase of oxidative stress (OS) related with ageing, genetics, recurrent inflammation, life style or carcinogens exposure as polycyclic aromatic hydrocarbons (PAHs). These last one are ubiquitous environmental contaminants resultant from the incomplete combustion of carbon-containing fuels such as tobacco, wood, diesel, or charbroiled [1,2].

Although numerous studies have related polycyclic aromatic hydrocarbons (PAHs) to tumour formation, few investigations have addressed PAHs effects on prostate cancer progression. Here we investigated the effect of four PAHs namely, pyrene, benzo(a)pyrene, chrysene and benzo(k)fluoranthene on cell growth and cell cycle progression, viability, mitochondria membrane potential, reactive oxygen species (ROS) production, vascular endothelial growth factor (VEGF) and hypoxia inducible factor (HIF) expression in the prostate cancer cell line, PC3, derived from bone metastasis.

Our data demonstrated that PAHs can stimulate cell growth, in line with an increase of the S-phase of the cell cycle, and mitochondria membrane potential. These results are also concomitant with an increase in VEGF and HIF expression and ROS levels, usually implicated in cancer progression, suggesting that PAHs can contribute to a more aggressive prostate cancer phenotype.

References

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    Biochim Biophys Acta 2009, 1795:83-91. PubMed Abstract | Publisher Full Text OpenURL

  2. Nelson WG, DeMarzo AM, Isaacs WB: Mechanisms of disease - prostate cancer.

    N Engl J Med 2003, 349:366-381. PubMed Abstract | Publisher Full Text OpenURL