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Characterization of an in vitro model to study the possible role of polyomavirus BK in prostate cancer


Villani, Sonia; Gagliano, Nicoletta; Procacci, Patrizia; Sartori, Patrizia; Comar, Manola; Provenzano, Maurizio; Favi, Evaldo; Ferraresso, Mariano; Ferrante, Pasquale; Delbue, Serena (2019). Characterization of an in vitro model to study the possible role of polyomavirus BK in prostate cancer. Journal of Cellular Physiology, 234(7):11912-11922.

Abstract

Prostate cancer (PCa) is the most common male neoplasms in the Western world. Various risk factors may lead to carcinogenesis, including infectious agents such as polyomavirus BK (BKPyV), which infects the human renourinary tract, establishes latency, and encodes oncoproteins. Previous studies suggested that BKPyV plays a role in PCa pathogenesis. However, the unspecific tropism of BKPyV and the lack of in vitro models of BKPyV‐infected prostate cells cast doubt on this hypothesis. The aim of the present study was to determine whether BKPyV could (a) infect normal and/or tumoral epithelial prostate cells and (b) affect their phenotype. Normal epithelial prostate RWPE‐1 cells and PCa PC‐3 cells were infected with BKPyV for 21 days. Cell proliferation, cytokine production, adhesion, invasion ability, and epithelial‐to‐mesenchymal transition (EMT) markers were analyzed. Our results show that (a) RWPE‐1 and PC‐3 cells are both infectable with BKPyV, but the outcome of the infection varies, (b) cell proliferation and TNF‐α production were increased in BKPyV‐infected RWPE‐1, but not in PC‐3 cells, (c) adhesion to matrigel and invasion abilities were elevated in BKPyV‐infected RWPE‐1 cells, and (d) loss of E‐cadherin and expression of vimentin occurred in both uninfected and infected RWPE‐1 cells. In conclusion, BKPyV may change some features of the normal prostate cells but is not needed for maintaining the transformed phenotype in the PCa cells The fact that RWPE‐1 cells exhibit some phenotype modifications related to EMT represents a limit of this in vitro model.

Abstract

Prostate cancer (PCa) is the most common male neoplasms in the Western world. Various risk factors may lead to carcinogenesis, including infectious agents such as polyomavirus BK (BKPyV), which infects the human renourinary tract, establishes latency, and encodes oncoproteins. Previous studies suggested that BKPyV plays a role in PCa pathogenesis. However, the unspecific tropism of BKPyV and the lack of in vitro models of BKPyV‐infected prostate cells cast doubt on this hypothesis. The aim of the present study was to determine whether BKPyV could (a) infect normal and/or tumoral epithelial prostate cells and (b) affect their phenotype. Normal epithelial prostate RWPE‐1 cells and PCa PC‐3 cells were infected with BKPyV for 21 days. Cell proliferation, cytokine production, adhesion, invasion ability, and epithelial‐to‐mesenchymal transition (EMT) markers were analyzed. Our results show that (a) RWPE‐1 and PC‐3 cells are both infectable with BKPyV, but the outcome of the infection varies, (b) cell proliferation and TNF‐α production were increased in BKPyV‐infected RWPE‐1, but not in PC‐3 cells, (c) adhesion to matrigel and invasion abilities were elevated in BKPyV‐infected RWPE‐1 cells, and (d) loss of E‐cadherin and expression of vimentin occurred in both uninfected and infected RWPE‐1 cells. In conclusion, BKPyV may change some features of the normal prostate cells but is not needed for maintaining the transformed phenotype in the PCa cells The fact that RWPE‐1 cells exhibit some phenotype modifications related to EMT represents a limit of this in vitro model.

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Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Urological Clinic
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Life Sciences > Physiology
Life Sciences > Clinical Biochemistry
Life Sciences > Cell Biology
Uncontrolled Keywords:Clinical Biochemistry, Cell Biology, Physiology
Language:English
Date:July 2019
Deposited On:11 Dec 2018 16:46
Last Modified:29 Jul 2020 08:22
Publisher:Wiley-Blackwell Publishing, Inc.
ISSN:0021-9541
OA Status:Green
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1002/jcp.27871
PubMed ID:30515818

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