PMID:12419962

Citation	Minamitani, T, Ariga, H and Matsumoto, K (2002) Adhesive defect in extracellular matrix tenascin-X-null fibroblasts: a possible mechanism of tumor invasion. Biol. Pharm. Bull. 25:1472-5
Abstract	Extracellular matrix tenascin-X (TNX)-null mice, generated by disruption of the Tnx gene, display augmented invasion and metastasis of B16-BL6 melanoma tumor cells due to increased activities of matrix metalloproteinase (MMP)-2 and MMP-9. In this study, we investigated cell-matrix and cell-cell adhesions using TNX-null fibroblasts and wild-type fibroblasts. TNX-null fibroblasts exhibited a decreased attachment to fibronectin compared with that of wild-type fibroblasts. B16 melanoma cells were cocultured with wild-type or TNX-null fibroblasts, and the adhesion of B16 melanoma to the fibroblasts was assessed. B16 melanoma cells on wild-type fibroblasts proliferated and spread out in a horizontal direction, whereas those on TNX-null fibroblasts overlapped each other rather than migrating horizontally. These overlapping B16 melanoma cells on TNX-null fibroblasts peeled off faster than those on wild-type fibroblasts. To determine whether the decreased cell-matrix and cell-cell adhesions on TNX-null fibroblasts were due to increased MMP activity, the activities of MMPs in wild-type and TNX-null fibroblasts were compared by gelatinolytic assays. The analysis of MMPs from conditioned media demonstrated that almost the same levels of MMP activities were detected between wild-type and TNX-null fibroblasts. However, contrary to our expectations the activities of MMPs from conditioned media of B16 melanoma cells cocultured on TNX-null fibroblasts were rather reduced than those of B16 melanoma cells cocultured on wild-type. We concluded that the absence of TNX in the extracellular environment might play an important role in enhancement of the detachment of B16 melanoma cells.
Links	PubMed
Keywords	Animals; Cell Adhesion/genetics; Coculture Techniques/methods; Extracellular Matrix/genetics; Extracellular Matrix/metabolism; Fibroblasts/metabolism; Melanoma, Experimental/genetics; Melanoma, Experimental/metabolism; Melanoma, Experimental/pathology; Mice; Mice, Inbred C57BL; Mice, Inbred CBA; Mice, Inbred ICR; Mice, Knockout; Neoplasm Invasiveness/genetics; Neoplasm Invasiveness/pathology; Tenascin/deficiency; Tenascin/genetics; Tumor Cells, Cultured
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