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 (P < 0.0001). 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.
Highlights
Prostate cancer is a form of cancer that develops in the male reproductive system often as slow growing mass before it is transformed to a malignant state; at this stage, the cancerous growth and tumor mass may become more aggressive [1, 2]
To understand why exposure to LPS would result in significant increase in prostate specific antigen” (PSA) secretion; since LPS is a known stimulant for inflammation, we proposed that infiltrating inflammatory molecules and change in the redox state of prostate microenvironment might induce a hypoxia similar to that found in solid tumor and could compromise the genomic stability of the epithelia cells, resulting in programming of the cells to a phenotype with cancer-like behaviors, including increase in PSA secretion
Available evidence suggests that the burden of prostate cancer in West African including Nigeria and Ghana is very high [16]
Summary
Prostate cancer is a form of cancer that develops in the male reproductive system often as slow growing mass before it is transformed to a malignant state; at this stage, the cancerous growth and tumor mass may become more aggressive [1, 2]. Recent studies have shown that Africa American men have the highest mortality rate of prostate cancer compared to any other racial or ethnic group in [6]. The study clearly showed higher rate of prostate cancer in West Africa. Data from the Laboratory of the authors clearly suggest that lack of access to antibiotics and presence of chronic inflammatory molecules might be associated with prostate cancer risk. We propose that increasing incidence of prostate cancer among West African men [6] might be due to constant exposure to microbial infection, which might induce inflammation-mediated hypoxia-driven cancer-like behaviors in the prostate. An experimental model was developed to investigate if exposure to microbial inflammatory molecule is linked to alteration in prostatic epithelia cell phenotype and cancer like behavior. We show that chronic local exposure prostate to lipopolysaccharide and superoxide resulted in increased PSA secretion, indicating a trend to prostate cancer transformation
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