alexa Monocyte-Induced Prostate Cancer Cell Invasion is Mediated by Chemokine ligand 2 and Nuclear Factor-and#195;and#381;and#194;and#186;B Activity | OMICS International | Abstract
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Review Article

Monocyte-Induced Prostate Cancer Cell Invasion is Mediated by Chemokine ligand 2 and Nuclear Factor-κB Activity

Paul F Lindholm1*, Neela Sivapurapu2, Borko Jovanovic3 and André Kajdacsy-Balla4
1Department of Pathology, Northwestern University, The Feinberg School of Medicine, Chicago, USA
2Indigenèse Biotechnologies, Hyderabad, India
3Department of Preventive Medicine and Bioinformatics Core, Northwestern University, The Feinberg School of Medicine, Chicago, USA
4Department of Pathology, University of Illinois at Chicago College of Medicine, Chicago, USA
Corresponding Author : Paul F Lindholm
Department of Pathology
Northwestern University
The Feinberg School of Medicine
303 East Chicago Avenue, Chicago, IL 60611, USA
Tel: 312-926-8483
Fax: 312-503-8249
E-mail: [email protected]
Received February 16, 2015; Accepted March 30, 2015; Published April 05, 2015
Citation: Lindholm PF, Sivapurapu N, Jovanovic B, Kajdacsy-Balla A (2015) Monocyte-Induced Prostate Cancer Cell Invasion is Mediated by Chemokine ligand 2 and Nuclear Factor-?B Activity. J Clin Cell Immunol 6:308. doi: 10.4172/2155-9899.1000308
Copyright: © 2015 Lindholm PF, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Study Background: The tumor microenvironment contains inflammatory cells which can influence cancer growth and progression; however the mediators of these effects vary with different cancer types. The mechanisms by which prostate cancer cells communicate with monocytes to promote cancer progression are incompletely understood. This study tested prostate cancer cell and monocyte interactions that lead to increased prostate cancer cell invasion. Methods: We analyzed the prostate cancer cell invasion and NF-κB activity and cytokine expression during interaction with monocyte-lineage cells in co-cultures. The roles of monocyte chemotactic factor (MCP-1/CCL2) and NF-κB activity for co-culture induced prostate cancer invasion were tested. Clinical prostate cancer NF-κB expression was analyzed by immunohistochemistry. Results: In co-cultures of prostate cancer cell lines with monocyte-lineage cells, (C-C motif) ligand 2 (CCL2) levels were significantly increased when compared with monocytes or cancer cells cultured alone. Prostate cancer cell invasion was induced by recombinant CCL2 in a dose dependent manner, similar to co-cultures with monocytes. The monocyte-induced prostate cancer cell invasion was inhibited by CCL2 neutralizing antibodies and by the CCR2 inhibitor, RS102895. Prostate cancer cell invasion and CCL2 expression induced in the co-cultures was inhibited by Lactacystin and Bay11-7082 NF-κB inhibitors. Prostate cancer cell NF-κB DNA binding activity depended on CCL2 dose and was inhibited by CCL2 neutralizing antibodies. Clinical prostate cancer NF-κB expression correlated with tumor grade. Conclusions: Co-cultures with monocyte-lineage cell lines stimulated increased prostate cancer cell invasion through increased CCL2 expression and increased prostate cancer cell NF-κB activity. CCL2 and NF-κB may be useful therapeutic targets to interfere with inflammation-induced prostate cancer invasion.

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