Macrophage Inflammatory Protein-2 Contributes to Liver Resection-induced Acceleration of Hepatic Metastatic Tumor Growth.
From: Department of General, Visceral, Vascular and Pediatric Surgery, University of the Saarland, D-66421 Homburg/Saar, Germany. chokol@uniklinik-saarland.de
World journal of gastroenterology : WJG
- Publish Date: Feb 2006
- ISSN: 1007-9327
- Volume: 12
- Issue: 6
- Pages: 858-67
- Medium: Print
- Language: English
- Citation (JAMA): Kollmar Otto, Menger Michael D, Schilling Martin K, et al. Macrophage Inflammatory Protein-2 Contributes to Liver Resection-induced Acceleration of Hepatic Metastatic Tumor Growth.. World J. Gastroenterol. Feb 2006;12:858-67
Abstract
AIM: To study the role of macrophage inflammatory protein (MIP)-2 in liver resection-induced acceleration of tumor growth in a mouse model of hepatic metastasis. METHODS: After a 50% hepatectomy, 1x10(5) CT26.WT cells were implanted into the left liver lobe of syngeneic balb/c mice (PHx). Additional animals were treated with a monoclonal antibody (MAB452) neutralizing MIP-2 (PHx+mAB). Non-resected and non-mAB-treated mice (Con) served as controls. After 7 d, tumor angiogenesis and microcirculation as well as cell proliferation, tumor growth, and CXCR-2 expression were analyzed using intravital fluorescence microscopy, histology, immunohistochemistry, and flow cytometry. RESULTS: Partial hepatectomy increased (P<0.05) the expression of the MIP-2 receptor CXCR-2 on tumor cells when compared with non-resected controls, and markedly accelerated (P<0.05) angiogenesis and metastatic tumor growth. Neutralization of MIP-2 by MAB452 treatment significantly (P<0.05) depressed CXCR-2 expression. Further, the blockade of MIP-2 reduced the angiogenic response (P<0.05) and inhibited tumor growth (P<0.05). Of interest, liver resection-induced hepatocyte proliferation was not effected by anti-MIP-2 treatment. CONCLUSION: MIP-2 significantly contributes to liver resection-induced acceleration of colorectal CT26.WT hepatic metastasis growth.
Mesh Headings (Keywords): Adenocarcinoma, Animals, Antibodies, Monoclonal, Cell Division, Chemokine CXCL2, Colorectal Neoplasms, Disease Models, Animal, Disease Progression, Flow Cytometry, Liver Neoplasms, Mice, Mice, Inbred BALB C, Microcirculation, Monokines, Neovascularization, Pathologic
Check for Full Text / PubMed Unique Identifier (PMID): 16521212
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