Abstract
RIT1, a member of the Ras family, has been identified as an oncogene in several malignancies. However, the expression and function of RIT1 in glioma remains to be addressed. In this study, we found RIT1 was upregulated in glioma and was associated with poor prognosis of glioma patients. Manipulating RIT1 levels in glioma cells via RNA interference significantly inhibited glioma cell proliferation and invasion in vitro whereas RIT1 overexpression exhibited the opposite effects. Mechanistically, we demonstrate that RIT1 engaged in the activation of the NF-ĸB pathway in vitro and in vivo. Furthermore, treating RIT1-overexpressing glioma cells with the p65 siRNA partially restrained their proliferation and invasion. Together these results indicate RIT1 contributes to the development and metastasis of glioma via the NF-ĸB pathway and suggest that targeting RIT1 may be a treatment strategy for this disease.