Background Glioblastoma (GBM) is an aggressive and malignant brain tumor with extremely poor prognosis. Despite advances in treatment, the pathogenesis of GBM remains elusive. Mounting studies have revealed the critical role of circular RNAs (circRNAs) in the development and progression of human cancers including GBM, but the comprehension of their functions is still insufficient. In this study, we investigated the expression profile of a circRNA derived from GLIS family zinc finger 3 (GLIS3) in GBM and normal astrocytes. CircGLIS3 expression was detected through quantitative real-time polymerase chain reaction (qRT-PCR) analysis. Functional experiments were performed to analyze the influence of circGLIS3 on GBM cell proliferation and apoptosis. In addition, mechanism assays were to uncover the potential regulatory mechanism of circGLIS3. Results CircGLIS3 was up-regulated in GBM cells and knockdown of circGLIS3 significantly hampered proliferation and promoted apoptosis of GBM cells. Furthermore, circGLIS3 positively regulated CAPG and GLIS3 by sponging miR-449c-5p to affect GBM cell proliferation and apoptosis. Conclusions In summary, our study identified that circGLIS3 could promote proliferation and inhibit apoptosis of GBM cells via targeting miR-449c-5p/GLIS3/CAPG axis in vitro. This study could offer a novel molecular perspective for further investigation into mechanisms essential to GBM progression.

Malignant glioma is one of the most common primary brain tumors and is among the deadliest of human cancers. In recent years, detection of related genes has provided a new perspective for early diagnosis and treatment of glioma. Previous studies have shown that macrophage capping protein (gelsolin-like, CAPG) is highly expressed in tumor cells, but there have been very few studies on glioma cells. In our study, several candidate genes were identified by lentivirus-mediated RNAi technology, and the infected glioma U251 cells were detected by qRT-PCR using Cellomics Highly Intensive Functional Screening (HCS) platform. The results showed that after knockdown of CAPG, the expression of CAPG gene in U251 glioma cells decreased, cell cycle was blocked, the number of U251 cells decreased, and the apoptotic rate increased. These results suggested that CAPG is significantly associated with the development of glioma cells. Shortening of CAPG inhibited the proliferation of glioma cells. CAPG could be used as an important reference for predicting the occurrence and development of glioma, and it could also serve as a novel target of targeted therapy for glioma.