Tumor necrosis factor α promotes invasiveness of cholangiocarcinoma cells via its receptor, TNFR2
Copyright policy )Tumor necrosis factor α promotes invasiveness of cholangiocarcinoma cells via its receptor, TNFR2
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-alpha substantially activated NFkappaB, 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.
- Nagoya University Japan
- Memorial Hospital of South Bend United States
- Tokai National Higher Education and Research System Japan
- Kanazawa University Japan
Tumor Necrosis Factor-alpha, NF-kappa B, Protein Serine-Threonine Kinases, Cholangiocarcinoma, Enzyme Activation, Matrix Metalloproteinase 9, Proto-Oncogene Proteins, Tumor Cells, Cultured, Humans, Receptors, Tumor Necrosis Factor, Type II, Neoplasm Invasiveness, Mitogen-Activated Protein Kinases, Proto-Oncogene Proteins c-akt
Tumor Necrosis Factor-alpha, NF-kappa B, Protein Serine-Threonine Kinases, Cholangiocarcinoma, Enzyme Activation, Matrix Metalloproteinase 9, Proto-Oncogene Proteins, Tumor Cells, Cultured, Humans, Receptors, Tumor Necrosis Factor, Type II, Neoplasm Invasiveness, Mitogen-Activated Protein Kinases, Proto-Oncogene Proteins c-akt
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