TRAIL induces MMP-9 expression via ERK activation in human astrocytoma cells
- Authors
- Kim, Jong-Hyun; Choi, Chulhee; Benveniste, Etty N.; Kwon, Daeho
- Issue Date
- 5-12월-2008
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- TRAII; MMP-9; ERK; NF-kappa B; Human astrocytoma cells
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.377, no.1, pp.195 - 199
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 377
- Number
- 1
- Start Page
- 195
- End Page
- 199
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/122240
- DOI
- 10.1016/j.bbrc.2008.09.095
- ISSN
- 0006-291X
- Abstract
- Matrix metalloproteinase-9 (MMP-9) is an Important angiogenic and prognostic factor ill malignant tumors. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is known as the death ligand, which induces preferential apoptosis of transformed tumor cells. In this study, we investigated the biological functions of TRAIL, other than its role in induction of apoptosis. We demonstrated that TRAIL induces MMP-9 expression in human astrocytoma cells, which is preceded by activation of extracellular signal-regulated protein kinase (ERK). In addition, TRAIL induces the DNA-binding activity of NF-kappa B, an important transcription factor for MMP-9 induction. The specific MEK Inhibitor, U0126, significantly blocks TRAIL-mediated NF-kappa B activation and subsequent MMP-9 induction. These findings indicate that TRAIL treatment in human astrocytoma cells leads to the activation of NF-kappa B and Subsequent expression of MMP-9, which are dependent oil ERK activation. Collectively, these results suggest that TRAIL has alternative biological functions in addition to its role ill inducing apoptosis in human malignant astrocytoma cells. (C) 2008 Elsevier Inc. All rights reserved.
- Files in This Item
- There are no files associated with this item.
- Appears in
Collections - ETC > 1. Journal Articles
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.