LAUSR

BACKGROUND Gliomas, the most common and malignant primary tumors, relate to the highest mortality rate of all central nervous system cancers. Previously, it has been demonstrated that Rap2A plays an essential role in tumor growth in human cancer cell lines. However, it remains largely unclear as to whether and how Rap2A is involved in the development of gliomas. In the current study, the role of Rap2A in glioma and its specific molecular mechanism are investigated by our group. METHODS Expression of Rap2A was examined in glioma cell lines and human normal astrocyte cells using Western blot analysis. Using the CCK-8 cell proliferation assay, wound healing assay, and transwell migration assay, we elucidated the role of Rap2A in glioma cell proliferation and migration. Levels of E-cadherin, vimentin and phosphorylation of ERK1/2 were also determined using Western blot. RESULTS The results suggested that Rap2A expression was remarkably decreased in glioma cells compared to the normal astrocyte cells. Overexpression of Rap2A prominently suppressed cell proliferation and migration as well as enhanced E-cadherin expression and reduced vimentin level in both U87 and U251 cells. In vivo assay proved that Rap2A overexpression slowed tumor growth of glioma. In particular, Rap2A overexpression remarkably inhibited ERK1/2 phosphorylation. CONCLUSIONS Therefore, our findings demonstrated that Rap2A functioned as a tumor suppressor via modulating the ERK1/2 signaling pathway, which may be a potential therapeutic candidate for treating glioma.