Paxillin functions as an oncogene in human gliomas by promoting cell migration and invasion.

Abstract

BackgroundPaxillin is implicated in tumorigenesis, progression and aggressive phenotypes of various malignancies, highlighting its functions in cellular adhesion, migration and survival. However, the roles of paxillin in human gliomas remain unclear. The aim of this study was to evaluate the clinical implication of paxillin expression in patients with gliomas and its biological function in glioma cells.Patients and methodsExpression levels of paxillin gene and protein, respectively, were detected by quantitative real-time reverse transcription polymerase chain reaction, Western blot and immunohistochemistry analyses in 120 pairs of glioma and matched nontumorous brain tissues. The associations between paxillin expression and various histopathological features of glioma patients were also statistically evaluated. Then, the functions of paxillin in cell migration and invasion of glioma cell lines were determined by transwell assays in vitro.ResultsThe expression levels of both paxillin gene and protein in glioma tissues were markedly higher than those in matched nontumorous brain tissues. Notably, paxillin overexpression was significantly associated with the grade of malignancy (P<0.05). Moreover, the enforced expression of paxillin promoted the migration and invasion of glioma cells, while the loss of paxillin expression efficiently suppressed cell migration and invasion of glioma cell lines.ConclusionOur data suggest that paxillin may function as an oncogene and its overexpression may be closely correlated with tumor progression of human gliomas by modulating tumor cell motility, implying the potential of paxillin as a new therapeutic target for glioma intervention.