The assessment of a possible link between HPV-mediated inflammation, apoptosis, and angiogenesis in Prostate cancer.


Journal

International immunopharmacology
ISSN: 1878-1705
Titre abrégé: Int Immunopharmacol
Pays: Netherlands
ID NLM: 100965259

Informations de publication

Date de publication:
Nov 2020
Historique:
received: 16 07 2020
revised: 14 08 2020
accepted: 15 08 2020
pubmed: 6 9 2020
medline: 28 5 2021
entrez: 5 9 2020
Statut: ppublish

Résumé

The aim of this study was to determine the presence of HPV in patients with Prostate cancer (PCa) and its possible association with cancer progression. In this case-control study, fresh prostate tissues and blood samples were collected from 90 individuals, including 58 cases samples with PCa and 32 non-malignant prostate tissue samples as a control group. The expression level of viral genes (E2, E6, and E7) and cellular factors including tumor suppressor proteins (Rb and p53), anti-apoptotic mediators (Bcl-2 and survivin), and some mediators involved in inflammation and angiogenesis was evaluated. The presence of the HPV genome was identified in 19 out of the 58 cases (32.7%) and five out of the 32 controls (15.6%). However, there was not any statistically significant relationship between the presence of the HPV genome and PCa (OR = 2.63, 95% C.I = 0.89-7.91, P-value = 0.078). Moreover, the HPV high-risk genotypes 16 and 18 were detected in 47.4% and 31.6% of HPV-infected PCa tissues, respectively. The expression level of the tumor suppressor proteins (Rb and p53) significantly decreased in the HPV-infected samples compared to the HPV negative specimens (P-value = 0.01, P-value = 0.01, respectively). However, the expression level of the anti-apoptotic mediators and those involved in angiogenesis and inflammation significantly increased in the HPV-infected PCa group compared to the HPV-negative PCa and control groups (P-value < 0.05, respectively). Our study suggests that although it is not definitely known whether HPV causes PCa, this virus probably modulates PCa cell behavior by affecting inflammation, angiogenesis, and apoptosis mechanisms, which, in turn, promotes tumorigenesis.

Sections du résumé

BACKGROUND BACKGROUND
The aim of this study was to determine the presence of HPV in patients with Prostate cancer (PCa) and its possible association with cancer progression.
METHODS METHODS
In this case-control study, fresh prostate tissues and blood samples were collected from 90 individuals, including 58 cases samples with PCa and 32 non-malignant prostate tissue samples as a control group. The expression level of viral genes (E2, E6, and E7) and cellular factors including tumor suppressor proteins (Rb and p53), anti-apoptotic mediators (Bcl-2 and survivin), and some mediators involved in inflammation and angiogenesis was evaluated.
RESULTS RESULTS
The presence of the HPV genome was identified in 19 out of the 58 cases (32.7%) and five out of the 32 controls (15.6%). However, there was not any statistically significant relationship between the presence of the HPV genome and PCa (OR = 2.63, 95% C.I = 0.89-7.91, P-value = 0.078). Moreover, the HPV high-risk genotypes 16 and 18 were detected in 47.4% and 31.6% of HPV-infected PCa tissues, respectively. The expression level of the tumor suppressor proteins (Rb and p53) significantly decreased in the HPV-infected samples compared to the HPV negative specimens (P-value = 0.01, P-value = 0.01, respectively). However, the expression level of the anti-apoptotic mediators and those involved in angiogenesis and inflammation significantly increased in the HPV-infected PCa group compared to the HPV-negative PCa and control groups (P-value < 0.05, respectively).
CONCLUSION CONCLUSIONS
Our study suggests that although it is not definitely known whether HPV causes PCa, this virus probably modulates PCa cell behavior by affecting inflammation, angiogenesis, and apoptosis mechanisms, which, in turn, promotes tumorigenesis.

Identifiants

pubmed: 32889239
pii: S1567-5769(20)32419-X
doi: 10.1016/j.intimp.2020.106913
pii:
doi:

Substances chimiques

Cytokines 0
DNA, Viral 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

106913

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Javid Sadri Nahand (J)

Department of Virology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran; Student Research Committee, Iran University of Medical Sciences, Tehran, Iran.

Maryam Esghaei (M)

Department of Virology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.

Seyed Hamidreza Monavari (S)

Department of Virology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.

Mohsen Moghoofei (M)

Department of Microbiology, Faculty of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran.

Seyed Jalal Kiani (S)

Department of Virology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.

Shayan Mostafaei (S)

Department of Biostatistics, Faculty of Health, Kermanshah University of Medical Sciences, Kermanshah, Iran.

Hamed Mirzaei (H)

Research Center for Biochemistry and Nutrition in Metabolic Diseases, Institute for Basic Sciences, Kashan University of Medical Sciences, Kashan, Iran.

Farah Bokharaei-Salim (F)

Department of Virology, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran. Electronic address: bokharaei.f@iums.ac.ir.

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Classifications MeSH