p21WAF1 mediates the IL-15-induced migration and invasion of human bladder cancer 5637 cells via the ERK1/2/NF-kappa B/MMP-9 pathway
- Authors
- Park, Sung Lyea; Kim, Wun-Jae; Moon, Sung-Kwon
- Issue Date
- Sep-2014
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- IL-15; Bladder cancer cells; Migration; Invasion; p21WAF1
- Citation
- INTERNATIONAL IMMUNOPHARMACOLOGY, v.22, no.1, pp 59 - 65
- Pages
- 7
- Journal Title
- INTERNATIONAL IMMUNOPHARMACOLOGY
- Volume
- 22
- Number
- 1
- Start Page
- 59
- End Page
- 65
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/11850
- DOI
- 10.1016/j.intimp.2014.06.008
- ISSN
- 1567-5769
1878-1705
- Abstract
- Interleukin-15 (IL-15) functions as a key regulator for the proliferation, differentiation, and activation of lymphocytes. However, the role of IL-15 in cancer biology is not yet understood. In the present study, IL-15 treatment stimulated the wound-healing migration and invasion of bladder cancer 5637 cells, without altering the proliferation of the cells. Treatment of 5637 cells with IL-15 resulted in the promotion of the MMP-9 expression and the activation of NF-kappa B binding, which is a functional transcription factor that activates MMP-9 expression. In addition, IL-15 induced the activation of ERK1/2. ERK inhibitor U0126 suppressed the migration, invasion, MMP-9 expression, and NF-kappa B binding activity in IL-15-treated 5637 cells. In addition, the cell-cycle inhibitor p21WAF1 was induced by the addition of IL-15. Finally, the siRNA-mediated knockdown of p21WAF1 attenuated the IL-15-induced stimulation of migration, invasion, ERK1/2 activation, MMP-9 expression, and NF-kappa B binding activation in 5637 cells. Our results suggest that p21WAF1 regulated NF-kappa B-mediated MMP-9 expression via the activation of ERK1/2, which resulted in the migration and invasion of 5637 cells treated with IL-15. These unexpected results suggest a potential role for IL-15 with respect to the progression of bladder cancer. (C) 2014 Published by Elsevier B.V.
- Files in This Item
-
- Appears in
Collections - ETC > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.