Tumor necrosis factor α promotes invasiveness of cholangiocarcinoma cells via its receptor, TNFR2

被引：48
|
作者：
Tanimura, Y
Kokuryo, T
Tsunoda, N
Yamazaki, Y
Oda, K
Nimura, Y
Mon, NN
Huang, PY
Nakanuma, Y
Chen, MF
Jan, YY
Yeh, TS
Chiu, CT
Hsieh, LL
Hamaguchi, M
机构：
[1] Nagoya Univ, Grad Sch Med, Div Canc Biol, Showa Ku, Nagoya, Aichi 4668550, Japan
[2] Nagoya Univ, Grad Sch Med, Dept Surg, Div Surg Oncol,Showa Ku, Nagoya, Aichi 4668550, Japan
[3] Kanazawa Univ, Grad Sch Med, Dept Human Pathol, Kanazawa, Ishikawa 9208641, Japan
[4] Chang Gumg Univ, Mem Hosp, Dept Surg, Taipei 105, Taiwan
[5] Chang Gumg Univ, Mem Hosp, Dept Gastroenterol, Taipei 105, Taiwan
[6] Chang Gumg Univ, Mem Hosp, Dept Publ Hlth, Taipei 105, Taiwan
来源：
CANCER LETTERS | 2005年 / 219卷 / 02期
关键词：
cholangiocarcinoma; matrix metalloproteinase; tumor necrosis factor-alpha; invasion;
D O I：
10.1016/j.canlet.2004.07.027
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
We studied the effect of TNF-alpha stimulation on a cholangiocarcinoma cell line, CCKS1. CCKS1 expressed only one type TNF receptor,TNFR2. Treatment of CCKS1 with TNF-a substantially activated NF kappa B, MAPK and Akt signalings which in turn activated matrix metalloproteinase-9 (MMP-9) secretion and in vitro invasiveness of CCKS1. Pretreatment of cells with anti-TNFR2 neutralizing antibody inhibited the TNF-alpha-dependent signaling and MMP-9 secretion and subsequently blocked invasion in vitro. Moreover, an inhibitor for matrix metalloproteinase, Galardin, suppressed the invasion in a dose-dependent manner. Similarly, pharmacological inhibition of signaling clearly suppressed the TNF-alpha dependent MMP-9 secretion. These results strongly suggest that TNF-alpha-TNFR2 signaling plays an important role to convert the cholangiocarcinoma cells to be more aggressive one. (c) 2004 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码：205 / 213
页数：9
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