Abstract
Despite advancements in neurosurgery, chemotherapy and radiation therapy, the outcome of patients with glioblastoma remains poor. The migration of tumor cells from the primary tumor site with subsequent invasion of these cells into the surrounding normal brain tissue is frequently responsible for relapse and treatment failure. The present study hypothesized that snail homolog 1 (SNAI1), a factor critically involved in the epithelial-mesenchymal transition (EMT) of human carcinoma cells, may also contribute to an invasive EMT-like phenotype of glioblastoma cells. The majority of glioblastoma cell lines investigated in the present study expressed SNAI1 at basal levels. The present study overexpressed SNAI1 in glioblastoma cell lines by lentiviral transfer of human SNAI1 complementary DNA. In addition, the inhibition of SNAI1 expression was achieved by lentiviral transfer of a short hairpin RNA specific for SNAI1. SNAI1 overexpression increased proliferation of one of the cell lines, U251MG, but exhibited only a weak effect on the migration and invasion of glioblastoma cells. However, downregulation of SNAI1 significantly decreased the invasive capacity of all investigated cell lines. In parallel, regained expression of E-cadherin, a marker that is usually lost during EMT, was observed subsequent to SNAI1 knockdown in the glioblastoma cell lines U87MG and U251MG. The data of the present study suggest that certain key genes of the EMT in carcinoma are also involved in the migration and invasion of human glioblastoma cells.