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BioMed Research International
Volume 2013 (2013), Article ID 791212, 11 pages
http://dx.doi.org/10.1155/2013/791212
Research Article

Mechanisms by Which Interleukin-6 Attenuates Cell Invasion and Tumorigenesis in Human Bladder Carcinoma Cells

1Department of Urology, Chang Gung Memorial Hospital, Kwei-Shan, Taoyuan 33305, Taiwan
2Bioinformation Center, Chang Gung Memorial Hospital, Kwei-Shan, Taoyuan 33305, Taiwan
3Department of Physiology, Collage of Medicine, Chang Gung University, Kwei-Shan, Taoyuan 33302, Taiwan
4Department of Anatomy, Collage of Medicine, Chang Gung University, Kwei-Shan, Taoyuan 33302, Taiwan
5School of Nursing, Collage of Medicine, Chang Gung University, Kwei-Shan, Taoyuan 33302, Taiwan

Received 25 March 2013; Accepted 23 April 2013

Academic Editor: Silvia Gregori

Copyright © 2013 Ke-Hung Tsui 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

Interleukin-6, a multifunctional cytokine, contributes to tumor cell proliferation and differentiation. However, the biological mechanisms that are affected by the expression of interleukin-6 in bladder cancer cells remain unclear. We evaluated the effects of interleukin-6 expression in human bladder carcinoma cells in vitro and in vivo. The results of interleukin-6-knockdown experiments in T24 cells and interleukin-6-overexpression experiments in HT1376 cells revealed that interleukin-6 reduced cell proliferation, migration, and invasion in vitro. Xenograft animal studies indicated that the overexpression of interleukin-6 downregulated tumorigenesis of bladder cells and that interleukin-6 knockdown reversed this effect. The results of RT-PCR, immunoblotting, and reporter assays indicated that the overexpression of interleukin-6 upregulated the expression of the mammary serine protease inhibitor (MASPIN), N-myc downstream gene 1 (NDRG1), and KAI1 proteins in HT1376 cells and that interleukin-6 knockdown reduced the expression of these proteins in T24 cells. In addition, results of immunoblotting assays revealed that interleukin-6 modulated epithelial-mesenchymal transitions by upregulating the expression of the E-cadherin, while downregulation N-cadherin and vimentin proteins. Our results suggest that the effects of interleukin-6 on the regulation of epithelial-mesenchymal transitions and the expressions of the MASPIN, NDRG1, and KAI1 genes attribute to the modulation of tumorigenesis in human bladder carcinoma cells.