MMP-26 is a novel member of the MMP family and is widely expressed in cancer cells of epithelial origin. Published research shows that MMP-26 contributes to tumor development and to the restoration of tissue injury. In this study, in order to identify the functions of MMP-26 that contribute to the biological phenotype and behavior of non-epithelial human glioma U251cells, we established an MMP-26 overexpressing tumor cell model using gene transfection. We then used these cells to investigate the role of MMP-26 in tumor progression. Adherence and spreading assay, wound healing assay, Boyden chamber invasion assay, and in vivo tumorigenicity assay were performed to analyze the invasion ability of MMP-26 transfected U251 cells. Microvessel density analysis and tumor cell induced angiogenesis assay were employed to detect the function of MMP-26 in angiogenesis. Results showed that the spreading cell ratio of MMP-26 transfected cells was significantly higher than parental U251 cells. The relative migration distance of MMP-26 transfected cells on Matrigel was significantly higher than that of parental U251 cells. The Boyden chamber assay showed that MMP-26 could significantly enhance the ability of U251 cells to invade through Matrigel. MMP-26 could also enhance the local invasion ability of U251 cells in vivo. There was a significant increase of the microvessel density of tumor tissue derived from MMP-26 transfected U251 cells. The vessel numbe induced by MMP-26 transfected U251 cells in nude mice was also significantly higher than that induced by parental U251 cells. In conclusion, we successfully established an MMP-26 overexpressing cell model and confirmed that MMP-26 contributed to U251 cell invasion and migration in vitro. We also demonstrated that MMP-26 plays an important role in local invasion, and angiogenesis.

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