Abstract | AIM: METHODS: The expression of CXCR4 and its signaling cascades were determined in the cholangiocarcinoma cell lines (RMCCA1 and KKU100) by Western blotting. The invasion assays and the detection of actin polymerization were tested in these cholangiocarcinoma cells treated with CXC chemokine ligand -12 (CXCL12). RESULTS: CONCLUSION: These results indicated that the activation of CXCR4 and its signaling pathways (MEK1/2 and Akt) are essential for CXCL12-induced cholangiocarcinoma cell invasion. This rises Implications on a potential role for the inhibition of CXCR4 or its signal cascades in the treatment of cholangiocarcinoma.
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Authors | Kawin Leelawat, Surang Leelawat, Siriluck Narong, Suradej Hongeng |
Journal | World journal of gastroenterology
(World J Gastroenterol)
Vol. 13
Issue 10
Pg. 1561-8
(Mar 14 2007)
ISSN: 1007-9327 [Print] United States |
PMID | 17461449
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Benzylamines
- Butadienes
- CXCL12 protein, human
- Chemokine CXCL12
- Chemokines, CXC
- Chromones
- Cyclams
- Enzyme Inhibitors
- Heterocyclic Compounds
- Morpholines
- Nitriles
- Phosphoinositide-3 Kinase Inhibitors
- Receptors, CXCR4
- U 0126
- 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
- Oncogene Protein v-akt
- MAP Kinase Kinase 1
- MAP Kinase Kinase 2
- plerixafor
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Topics |
- Benzylamines
- Bile Duct Neoplasms
(genetics, pathology, physiopathology)
- Bile Ducts, Intrahepatic
- Butadienes
(pharmacology)
- Cell Line, Tumor
- Chemokine CXCL12
- Chemokines, CXC
(genetics, physiology)
- Cholangiocarcinoma
(genetics, pathology, physiopathology)
- Chromones
(pharmacology)
- Cyclams
- Cytoskeleton
(physiology)
- Enzyme Inhibitors
(pharmacology)
- Gene Expression Regulation, Neoplastic
(physiology)
- Heterocyclic Compounds
(pharmacology)
- Humans
- MAP Kinase Kinase 1
(antagonists & inhibitors, genetics, physiology)
- MAP Kinase Kinase 2
(antagonists & inhibitors, genetics, physiology)
- Morpholines
(pharmacology)
- Neoplasm Invasiveness
(genetics, physiopathology)
- Nitriles
(pharmacology)
- Oncogene Protein v-akt
(genetics, physiology)
- Phosphatidylinositol 3-Kinases
(physiology)
- Phosphoinositide-3 Kinase Inhibitors
- Receptors, CXCR4
(antagonists & inhibitors, genetics, physiology)
- Signal Transduction
(physiology)
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