Long non-coding RNA SUMO1P3 promotes glioma progression via the Wnt/β-catenin pathway.

OBJECTIVE Long non-coding RNA SUMO1P3 has been reported to act as an oncogene in the tumorigenesis of several types of human malignancy. However, to the best of our knowledge, the exact biological functions and potential mechanism of lncRNA SUMO1P3 in glioma remains unknown. Therefore, the aim of this study was to investigate the potential role of SUMO1P3 in glioma and to explore the underlying mechanism. PATIENTS AND METHODS The present study examined SUMO1P3 expression in glioma tissues and cell lines using reverse transcription-quantitative polymerase chain reaction. Cell Counting Kit-8 (CCK-8) and transwell assays were used to examine the effects of SUMO1P3 on the proliferation and invasion of glioma cells, respectively. Furthermore, Western blot was used to detect the expression levels of proteins in the epithelial-mesenchymal transition (EMT) process. RESULTS The expression level of SUMO1P3 was higher in glioma tissues compared with corresponding adjacent normal tissues. In addition, a high expression level of SUMO1P3 was significantly associated with clinical progression and poor survival for patients with glioma. Furthermore, the knockdown of SUMO1P3 inhibited the proliferation, migration and invasion of U87 and U251 cells. In addition, the knockdown of SUMO1P3 inhibits glioma growth in vivo. Finally, the knockdown of SUMO1P3 inhibited the epithelial-mesenchymal transition and reduced the expression levels of active β-catenin, C-myc, and cyclin D1 in U87 and U251 cells. By contrast, the overexpression of SUMO1P3 promoted glioma cell proliferation, migration, and invasion. CONCLUSIONS SUMO1P3 promotes glioma cell proliferation, migration, and invasion, and may be involved in Wnt/β-catenin signaling.