Human Cytomegalovirus Infection Alters PC3 Prostate Carcinoma Cell Adhesion to Endothelial Cells, Extracellular Matrix

Neoplasia: An International Journal for Oncology Research

Jürgen Bereiter-Hahn¹  Roman A. Blaheta²  Eva Weich²  Dana Marian²  Jon Jones²  Dietger Jonas²  Martin Michaelis³  Jindrich Cinatl, Jr.³  Hans Willhelm Doerr³ 

[1] Institut für Kinematische Zellforschung, Fachbereich Biowissenschaften, Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany;Zentrum der Chirurgie, Klinik für Urologie und Kinderurologie, Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany;Zentrum der Hygiene, Institut für Medizinische Virologie, Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany;

关键词: Adhesion;    HCMV;    integrins;    oncomodulation;    prostate carcinoma cells;   

DOI  :  10.1593/neo.06379

来源: DOAJ

【 摘 要 】

The genome, 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, extracellular matrix proteins. Experiments were based on the human prostate tumor cell line PC3, either infected with the HCMV strain Hi (HCMVHi) or transfected with cDNA encoding the HCMV-specific immediate early protein IEA1 (UL123) or IEA2 (UL122). HCMVHi upregulated PC3 adhesion to the endothelium, to the extracellular matrix proteins collagen, laminin, fibronectin. The process was accompanied by enhancement of β1-integrin surface expression, elevated levels of integrin-linked kinase, phosphorylation of focal adhesion kinase. IEA1 or IEA2 did not modulate PC3 adhesion or β1-integrin expression. Based on this in vitro model, we postulate a direct association between HCMV infection, 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 PC3Hi 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.

【 授权许可】

Unknown