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 G... More
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.
