Yu 23/2

Telomerase activation is a common feature of most types of human cancers. Although several studies have shown that activation of telomerase might participate in the progression of tumors, the mechanism by which telomerase activation causes the invasion and metastasis of tumors remains unclear. In this study, we transfected a vector containing the full-length cDNA of hTERT into a telomerasenegative osteosarcoma cell line U2OS (hTERT/U2OS). Vacant vector-transfected U2OS cells served as a control (EGFP/U2OS). We then compared the biological and vitodynamic changes in these transfected and untransfected U2OS cells. The hTERT protein was detected in hTERT/U2OS cells by Western blot analysis and immunochemistry assay. The telomere length in hTERT/U2OS cells was longer than that in EGFP/U2OS and untransfected U2OS cells. We also found using vacuum micropipette aspiration that hTERT transfection did not only promote the proliferation of hTERT-transfected U2OS cells but also increased the cellular adhesion capacity to the extracellular matrix. Transwell matrigel assay confirmed an increased invasion ability in hTERT/U2OS cells. These results strongly suggest that hTERT transfection promotes the invasion of telomerase-negative cells. Telomerasemediated telomere maintenance enables these cells to achieve a fully malignant endpoint, including invasion and metastasis.