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Schistosoma Egg Antigen Induces Oncogenic Alterations in Human Prostate Cells
Schistosomiasis is a neglected tropical disease that affects 200 million people and accounts for 100,000 deaths annually. In endemic geographical areas, schistosomiasis has been implicated as an etiological agent in the pathogenesis of bladder, colorectal, and renal carcinoma largely due to Schistos...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6305059/ https://www.ncbi.nlm.nih.gov/pubmed/30631746 http://dx.doi.org/10.1155/2018/4675380 |
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author | Tuffour, Isaac Ayi, Irene Gwira, Theresa Manful Dumashie, Edward Ashong, Yvonne Appiah-Opong, Regina |
author_facet | Tuffour, Isaac Ayi, Irene Gwira, Theresa Manful Dumashie, Edward Ashong, Yvonne Appiah-Opong, Regina |
author_sort | Tuffour, Isaac |
collection | PubMed |
description | Schistosomiasis is a neglected tropical disease that affects 200 million people and accounts for 100,000 deaths annually. In endemic geographical areas, schistosomiasis has been implicated as an etiological agent in the pathogenesis of bladder, colorectal, and renal carcinoma largely due to Schistosoma eggs in tissues that comes with chronic infection. Several studies have also reported cases of association between Schistosoma infection and prostate cancer. The possible causal association is however poorly understood. We hypothesized in this study that infection of the prostate cells with Schistosoma spp promotes cancer. Urine samples from individuals living in Galilea, a schistosomiasis endemic community in the Ga South District of Ghana, were collected and screened for Schistosoma infection via microscopy and multiplex PCR. Soluble egg antigens (SEA) were prepared from Schistosoma egg-positive urine samples and assessed for the ability to induce cancer-like phenotypes including excessive proliferation, oxidative stress (reduced glutathione (GSH) depletion), and diminished apoptosis in cultured human prostate (PNT2) cells. Molecular analysis revealed infecting schistosome species to be S. haematobium and S. mansoni. Prostate cell proliferation was significantly induced by 12.5 μg/ml SEA (p = 0.029). Also, SEA dose-dependently depleted cellular GSH. Flow cytometric analysis and fluorescence staining revealed that SEA dose-dependently diminished apoptosis, significantly, in prostate cells. Findings of this study suggest that schistosome infection may play a role in the pathogenesis of prostate cancer. In vivo studies are however needed to confirm this association. |
format | Online Article Text |
id | pubmed-6305059 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-63050592019-01-10 Schistosoma Egg Antigen Induces Oncogenic Alterations in Human Prostate Cells Tuffour, Isaac Ayi, Irene Gwira, Theresa Manful Dumashie, Edward Ashong, Yvonne Appiah-Opong, Regina Anal Cell Pathol (Amst) Research Article Schistosomiasis is a neglected tropical disease that affects 200 million people and accounts for 100,000 deaths annually. In endemic geographical areas, schistosomiasis has been implicated as an etiological agent in the pathogenesis of bladder, colorectal, and renal carcinoma largely due to Schistosoma eggs in tissues that comes with chronic infection. Several studies have also reported cases of association between Schistosoma infection and prostate cancer. The possible causal association is however poorly understood. We hypothesized in this study that infection of the prostate cells with Schistosoma spp promotes cancer. Urine samples from individuals living in Galilea, a schistosomiasis endemic community in the Ga South District of Ghana, were collected and screened for Schistosoma infection via microscopy and multiplex PCR. Soluble egg antigens (SEA) were prepared from Schistosoma egg-positive urine samples and assessed for the ability to induce cancer-like phenotypes including excessive proliferation, oxidative stress (reduced glutathione (GSH) depletion), and diminished apoptosis in cultured human prostate (PNT2) cells. Molecular analysis revealed infecting schistosome species to be S. haematobium and S. mansoni. Prostate cell proliferation was significantly induced by 12.5 μg/ml SEA (p = 0.029). Also, SEA dose-dependently depleted cellular GSH. Flow cytometric analysis and fluorescence staining revealed that SEA dose-dependently diminished apoptosis, significantly, in prostate cells. Findings of this study suggest that schistosome infection may play a role in the pathogenesis of prostate cancer. In vivo studies are however needed to confirm this association. Hindawi 2018-12-09 /pmc/articles/PMC6305059/ /pubmed/30631746 http://dx.doi.org/10.1155/2018/4675380 Text en Copyright © 2018 Isaac Tuffour et al. http://creativecommons.org/licenses/by/4.0/ 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. |
spellingShingle | Research Article Tuffour, Isaac Ayi, Irene Gwira, Theresa Manful Dumashie, Edward Ashong, Yvonne Appiah-Opong, Regina Schistosoma Egg Antigen Induces Oncogenic Alterations in Human Prostate Cells |
title |
Schistosoma Egg Antigen Induces Oncogenic Alterations in Human Prostate Cells |
title_full |
Schistosoma Egg Antigen Induces Oncogenic Alterations in Human Prostate Cells |
title_fullStr |
Schistosoma Egg Antigen Induces Oncogenic Alterations in Human Prostate Cells |
title_full_unstemmed |
Schistosoma Egg Antigen Induces Oncogenic Alterations in Human Prostate Cells |
title_short |
Schistosoma Egg Antigen Induces Oncogenic Alterations in Human Prostate Cells |
title_sort | schistosoma egg antigen induces oncogenic alterations in human prostate cells |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6305059/ https://www.ncbi.nlm.nih.gov/pubmed/30631746 http://dx.doi.org/10.1155/2018/4675380 |
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