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BioMed Research International
Volume 2014, Article ID 536049, 16 pages
http://dx.doi.org/10.1155/2014/536049
Research Article

Cytokine Effects on Cell Viability and Death of Prostate Carcinoma Cells

1Department of Anatomy-Histology-Embryology, Medical School, University of Ioannina, 45110 Ioannina, Greece
2Laboratory of Hematology, University Hospital of Ioannina, 45500 Ioannina, Greece
3Department of Pathology, Medical School, University of Ioannina, 45110 Ioannina, Greece
4Department of Urology, Medical School, University of Ioannina, 45110 Ioannina, Greece
5Department of Anatomy, Medical School, University of Thessaly, 44110 Larisa, Greece

Received 15 February 2014; Revised 9 April 2014; Accepted 6 May 2014; Published 29 May 2014

Academic Editor: Gary E. Gallick

Copyright © 2014 Georgios Chondrogiannis et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

We analyzed the effects of IL-13, IFN-γ, and IL-1β on cell viability and death of LNCaP and PC-3 cells and major signaling pathways involved in these effects. Significant increase of LNCaP cell death (apoptotic and necrotic) and increased levels of active caspase 3 were observed in cells treated with inhibitors of ERK 1/2 (UO126) and p38 (SB203580) prior to IL-1β treatment in comparison to cells treated with UO126, SB203580, or IL-1β alone. Significant increase of LNCaP but not PC-3 cell death was detected after treatment with LY-294002 (inhibitor of phosphatidylinositol 3-kinase). No significant increase of LNCaP and PC-3 cell death was observed after treatment with SP600125 (inhibitor of JNK), SB203580 (inhibitor of p38), UO126 (inhibitor of ERK 1/2), or BAY 11-7082 (inhibitor of NF-κB). Reduced c- expression was observed in LNCaP cells treated with LY-294002. The significant potentiation of LNCaP cell death by inhibition of ERK 1/2, p38, and PI3-K pathways may provide a rationale for therapeutic approach in androgen-dependent prostate cancer.