Overexpression of EPAC2 reduces the invasion of glioma cells via MMP-2

Exchange proteins directly activated by cAMP (EPACs) are crucial cyclic adenosine 3,5-monophosphate- determined signaling pathway intercessors, which are associated with the pathogenesis of neurological disorders and numerous human diseases. To the best of our knowledge, the role of EPAC2 signaling via matrix metalloproteinase 2 (MMP-2) in the pathogenesis of glioma has not been studied. Therefore, the present study focused on the role of EPAC2 in glioma, and assessed the invasiveness of human glioma cell lines following EPAC2 overexpression. Expression levels of EPAC2 in normal brain tissues and clinical glioma specimens were detected by western blotting. An EPAC2 overexpression vector was transfected into U251 and U87 cell lines to increase the expression levels of EPAC2. Expression levels of MMP-2 were detected by western blotting, and the invasive abilities of glioma cells were detected by a Transwell assay. EPAC2 was relatively highly expressed in normal brain tissue, while EPAC2 expression was significantly decreased in clinical glioma specimens (P<0.01). In vitro transfection of EPAC2 overexpression vector significantly reduced the MMP-2 protein levels of glioma cells, and, at the same time, the invasive cell number was significantly decreased in a Transwell assay. The present study demonstrated that MMP-2 regulation via EPAC2 overexpression is a novel promising therapeutic route in malignant types of glioma.