Human cytomegalovirus infection alters PC3 prostate carcinoma cell adhesion to endothelial cells and extracellular matrix.

Blaheta, Roman A. and Weich, Eva and Marian, Dana and Bereiter-Hahn, Jürgen and Jones, Jon and Jonas, Dietger and Michaelis, Martin and Doerr, Hans Wilhelm and Cinatl, Jindrich (2006) Human cytomegalovirus infection alters PC3 prostate carcinoma cell adhesion to endothelial cells and extracellular matrix. Neoplasia, 8 (10). pp. 807-16. ISSN 1476-5586. (The full text of this publication is not currently available from this repository. You may be able to access a copy if URLs are provided)

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Abstract

The genome and antigens of human cytomegalovirus (HCMV) are frequently found in prostatic carcinoma. However, whether this infection is causative or is an epiphenomenon is not clear. We therefore investigated the ability of HCMV to promote metastatic processes, defined by tumor cell adhesion to the endothelium and extracellular matrix proteins. Experiments were based on the human prostate tumor cell line PC3, either infected with the HCMV strain Hi (HCMV(Hi)) or transfected with cDNA encoding the HCMV-specific immediate early protein IEA1 (UL123) or IEA2 (UL122). HCMV(Hi) upregulated PC3 adhesion to the endothelium and to the extracellular matrix proteins collagen, laminin, and fibronectin. The process was accompanied by enhancement of beta(1)-integrin surface expression, elevated levels of integrin-linked kinase, and phosphorylation of focal adhesion kinase. IEA1 or IEA2 did not modulate PC3 adhesion or beta(1)-integrin expression. Based on this in vitro model, we postulate a direct association between HCMV infection and prostate tumor transmigration, which is not dependent on IEA proteins. Integrin overexpression, combined with the modulation of integrin-dependent signalling, seems to be, at least in part, responsible for a more invasive PC3(Hi) tumor cell phenotype. Elevated levels of c-myc found in IEA1-transfected or IEA2-transfected PC3 cell populations might promote further carcinogenic processes through accelerated cell proliferation.

Item Type: Article
Subjects: Q Science > QR Microbiology > QR355 Virology
Divisions: Faculties > Sciences > School of Biosciences
Depositing User: Martin Michaelis
Date Deposited: 05 Jun 2013 20:55 UTC
Last Modified: 01 Jul 2014 15:48 UTC
Resource URI: https://kar.kent.ac.uk/id/eprint/34098 (The current URI for this page, for reference purposes)
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