2009年10月
NIK is involved in constitutive activation of the alternative NF-kappa B pathway and proliferation of pancreatic cancer cells
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
ダウンロード
回数 : 51
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- 巻
- 388
- 号
- 1
- 開始ページ
- 96
- 終了ページ
- 101
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1016/j.bbrc.2009.07.125
- 出版者・発行元
- ACADEMIC PRESS INC ELSEVIER SCIENCE
Pancreatic cancer has one of the poorest prognoses among human neoplasms. Constitutive activation of NF-kappa B is frequently observed in pancreatic cancer cells and is involved in their malignancy. However, little is known about the molecular mechanism of this constitutive NF-kappa B activation. Here, we show that the alternative pathway is constitutively activated and NF-kappa B-inducing kinase (NIK), a mediator of the alternative pathway, is significantly expressed in pancreatic cancer cells. siRNA-mediated silencing of NIK expression followed by subcellular fractionation revealed that NIK is constitutively involved in the processing of p100 and nuclear transport of p52 and RelB in pancreatic cancer cells. In addition, NIK silencing significantly suppressed proliferation of pancreatic cancer cells. These results clearly indicate that NIK is involved in the constitutive activation of the alternative pathway and controls cell proliferation in pancreatic cancer cells. Therefore, NIK might be a novel target for the treatment of pancreatic cancer. (C) 2009 Elsevier Inc. All rights reserved.
- リンク情報
- ID情報
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- DOI : 10.1016/j.bbrc.2009.07.125
- ISSN : 0006-291X
- eISSN : 1090-2104
- PubMed ID : 19646419
- SCOPUS ID : 68949097479
- Web of Science ID : WOS:000274534200019