肿瘤坏死因子α
基质金属蛋白酶
分泌物
癌症研究
受体
蛋白激酶B
体外
信号转导
MAPK/ERK通路
细胞培养
化学
细胞生物学
刺激
生物
医学
免疫学
内科学
内分泌学
生物化学
遗传学
作者
Yoko Tanimura,Toshio Kokuryo,Nobuyuki Tsunoda,Yukiko Yamazaki,Koji Oda,Yuji Nimura,Naing Naing Mon,Pengyu Huang,Yasuni Nakanuma,Min-Fu Chen,Yi-Yin Jan,Ta-Sen Yeh,Cheng-Taug Chiu,Ling–Ling Hsieh,Michinari Hamaguchi
出处
期刊:Cancer Letters
[Elsevier]
日期:2005-03-01
卷期号:219 (2): 205-213
被引量:54
标识
DOI:10.1016/j.canlet.2004.07.027
摘要
We studied the effect of TNF-α stimulation on a cholangiocarcinoma cell line, CCKS1. CCKS1 expressed only one type TNF receptor, TNFR2. Treatment of CCKS1 with TNF-α substantially activated NFκB, 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-α-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-α dependent MMP-9 secretion. These results strongly suggest that TNF-α-TNFR2 signaling plays an important role to convert the cholangiocarcinoma cells to be more aggressive one.
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