Table of Contents
International Scholarly Research Notices
Volume 2014 (2014), Article ID 420429, 6 pages
http://dx.doi.org/10.1155/2014/420429
Research Article

Exposure of Prostate to Lipopolysaccharide and Hypoxia Potentiates Neoplastic Behavior and Risk for Prostate Carcinogenesis In Vivo

1Department of Oncology, Cancer Research Division, University of Saskatchewan, Saskatoon, SK, Canada S7N 5R5
2Molecular Cancer Biology Research Group, Molecular Pathology and Immunology Division, Department of Medical Laboratory Sciences, School of Biomedical Science, Faculty of Health Science, Ebonyi State University, Abakaliki, Nigeria
3Department of Pathology and Molecular Medicine, University of Leicester, Leicester, UK

Received 20 April 2014; Accepted 9 June 2014; Published 17 August 2014

Academic Editor: Athanasios Papatsoris

Copyright © 2014 Maxwell Omabe et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

A number of studies showed that men from tropical countries have higher burden of prostate cancer similar to data from USA. We developed a translational model to examine whether exposure to microbial inflammation-inducing molecule lipopolysacchride LPS was associated with prostatic cell transformation to more proliferative phenotype as indicated by PSA secretion. Immunocompetent adult mice were divided into two groups; the first group received a local prostate inoculation with E. coli, while the second group received inoculation with sterile solution of saline as vehicle. At the end of 6 days, the PSA values were measured and compared. In the second experiment, two groups of animals were involved. The test group received two drops of the hydrogen peroxide orally for six to seven days to induce hypoxia, while the control group received normal saline. Blood samples were evaluated for serum level of PSA. Result showed a 2-fold increase in level of PSA compared to the control mice in the E. coli inoculated-LPS exposed animals. In addition, exposure of the animals to hypoxic stress resulted in 3.5 fold increase in the serum PSA compared to the control group, which was found to be statistically significant (). In conclusion, our data shows that chronic prostatic infection and exposure to inflammatory stimulus, especially LPS, may alter the phenotype of prostate epithelial cells for increased PSA secretion, a known cancer-like behavior; this is mediated by compromised redox state and oxidative stress injury. We propose that exposure of the prostate epithelial cells to lipopolysaccharide (LPS) promotes chronic inflammation and risk of neoplastic behavior of the prostate in vivo; this may explain the high rate of prostate cancer in tropics.