Artikel
Macrophage inflammatory protein (MIP)-2 contributes to liver resection-induced acceleration of hepatic metastatic tumor growth.
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Veröffentlicht: | 20. März 2006 |
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Gliederung
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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, 1 x 105 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 days, 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: Our study demonstrates that MIP-2 significantly contributes to liver resection-induced acceleration of colorectal CT26.WT hepatic metastasis growth.