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Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer

BACKGROUND: This study aimed to evaluate the possible role of human papillomavirus (HPV) and Epstein–Barr virus (EBV) coinfection as an etiological factor for prostate cancer (PCa) development. METHODS: This case-control study was conducted on 67 patients with PCa and 40 control subjects. The expres...

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Autores principales: Nahand, Javid Sadri, Khanaliha, Khadijeh, Mirzaei, Hamed, Moghoofei, Mohsen, Baghi, Hossein Bannazadeh, Esghaei, Maryam, Khatami, Ali Reza, Fatemipour, Maryam, Bokharaei-Salim, Farah
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8369687/
https://www.ncbi.nlm.nih.gov/pubmed/34399719
http://dx.doi.org/10.1186/s12885-021-08658-y
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author Nahand, Javid Sadri
Khanaliha, Khadijeh
Mirzaei, Hamed
Moghoofei, Mohsen
Baghi, Hossein Bannazadeh
Esghaei, Maryam
Khatami, Ali Reza
Fatemipour, Maryam
Bokharaei-Salim, Farah
author_facet Nahand, Javid Sadri
Khanaliha, Khadijeh
Mirzaei, Hamed
Moghoofei, Mohsen
Baghi, Hossein Bannazadeh
Esghaei, Maryam
Khatami, Ali Reza
Fatemipour, Maryam
Bokharaei-Salim, Farah
author_sort Nahand, Javid Sadri
collection PubMed
description BACKGROUND: This study aimed to evaluate the possible role of human papillomavirus (HPV) and Epstein–Barr virus (EBV) coinfection as an etiological factor for prostate cancer (PCa) development. METHODS: This case-control study was conducted on 67 patients with PCa and 40 control subjects. The expression levels of cellular and viral factors involved in inflammation, tumor progression, and metastasis were quantified, using the enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR) assay. RESULTS: The EBV/HPV coinfection was reported in 14.9% of patients in the case group and 7.5% of the control subjects. The high-risk types of HPV, that is, HPV 16 and HPV 18, were responsible for 50 and 30% of HPV/EBV-coinfected PCa cases (n = 10), respectively. No significant relationship was observed between PCa and HPV/EBV coinfection (OR = 2.9, 95% CI: 0.18–45.2, P = 0.31). However, the highest percentage of HPV genome integration was found in the HPV/EBV-coinfected PCa group (8/10; 80%). Also, the mean expression levels of inflammatory factors (IL-17, IL-6, TNF-α, NF-κB, VEGF, ROS, and RNS), anti-apoptotic mediators (Bcl-2 and survivin), and anti-anoikis factors (Twist and N-cadherin) were significantly higher in the HPV/EBV-coinfected PCa group, compared to the non-coinfected PCa cases. Nevertheless, the tumor-suppressor proteins (p53 and pRb) and E-cadherin (inhibitor of anoikis resistance) showed significant downregulations in the HPV/EBV-coinfected PCa group, compared to the non-coinfected PCa cases. CONCLUSION: The HPV/EBV coinfection may be an etiological factor for PCa through modulation of cellular behaviors. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12885-021-08658-y.
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spelling pubmed-83696872021-08-18 Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer Nahand, Javid Sadri Khanaliha, Khadijeh Mirzaei, Hamed Moghoofei, Mohsen Baghi, Hossein Bannazadeh Esghaei, Maryam Khatami, Ali Reza Fatemipour, Maryam Bokharaei-Salim, Farah BMC Cancer Research BACKGROUND: This study aimed to evaluate the possible role of human papillomavirus (HPV) and Epstein–Barr virus (EBV) coinfection as an etiological factor for prostate cancer (PCa) development. METHODS: This case-control study was conducted on 67 patients with PCa and 40 control subjects. The expression levels of cellular and viral factors involved in inflammation, tumor progression, and metastasis were quantified, using the enzyme-linked immunosorbent assay (ELISA) and quantitative real-time polymerase chain reaction (qRT-PCR) assay. RESULTS: The EBV/HPV coinfection was reported in 14.9% of patients in the case group and 7.5% of the control subjects. The high-risk types of HPV, that is, HPV 16 and HPV 18, were responsible for 50 and 30% of HPV/EBV-coinfected PCa cases (n = 10), respectively. No significant relationship was observed between PCa and HPV/EBV coinfection (OR = 2.9, 95% CI: 0.18–45.2, P = 0.31). However, the highest percentage of HPV genome integration was found in the HPV/EBV-coinfected PCa group (8/10; 80%). Also, the mean expression levels of inflammatory factors (IL-17, IL-6, TNF-α, NF-κB, VEGF, ROS, and RNS), anti-apoptotic mediators (Bcl-2 and survivin), and anti-anoikis factors (Twist and N-cadherin) were significantly higher in the HPV/EBV-coinfected PCa group, compared to the non-coinfected PCa cases. Nevertheless, the tumor-suppressor proteins (p53 and pRb) and E-cadherin (inhibitor of anoikis resistance) showed significant downregulations in the HPV/EBV-coinfected PCa group, compared to the non-coinfected PCa cases. CONCLUSION: The HPV/EBV coinfection may be an etiological factor for PCa through modulation of cellular behaviors. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12885-021-08658-y. BioMed Central 2021-08-17 /pmc/articles/PMC8369687/ /pubmed/34399719 http://dx.doi.org/10.1186/s12885-021-08658-y Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Nahand, Javid Sadri
Khanaliha, Khadijeh
Mirzaei, Hamed
Moghoofei, Mohsen
Baghi, Hossein Bannazadeh
Esghaei, Maryam
Khatami, Ali Reza
Fatemipour, Maryam
Bokharaei-Salim, Farah
Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer
title Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer
title_full Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer
title_fullStr Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer
title_full_unstemmed Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer
title_short Possible role of HPV/EBV coinfection in anoikis resistance and development in prostate cancer
title_sort possible role of hpv/ebv coinfection in anoikis resistance and development in prostate cancer
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8369687/
https://www.ncbi.nlm.nih.gov/pubmed/34399719
http://dx.doi.org/10.1186/s12885-021-08658-y
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