Conclusion
Our results verified the involvement of the LINC01094/miR-577/BDNF pathway in GBM cells and its enhancing effects on the aggressive behaviors of GBM cells in vitro and in vivo. This pathway may be a novel and promising focus for the future development of targeted therapies for GBM.
Methods
LINC01094 expression in GBM was determined with quantitative reverse transcription polymerase chain reaction. The proliferation, apoptosis, migration, invasion in vitro, and tumor growth in vivo of GBM cells were evaluated using Cell Counting Kit-8 assay, flow cytometry analysis, migration assay, invasion assay, and tumor xenograft models, respectively.
Purpose
The long intergenic non-protein coding RNA 1094 (LINC01094) plays a vital role in the oncogenicity of clear cell renal cell carcinoma. However, its expression profile and detailed roles in glioblastoma (GBM) remain unknown. In this study, we mainly investigated the expression and roles of LINC01094 in GBM and focused on the mechanism by which LINC01094 regulates the malignant characteristics of GBM. Patients and
Results
LINC01094 was overexpressed in GBM tissues and cell lines. Moreover, increased LINC01094 expression was associated with adverse clinicopathological parameters in patients with GBM. Loss of LINC01094 inhibited GBM cell proliferation, migration, and invasion; promoted cell apoptosis; and suppressed tumor growth in vivo. Mechanically, LINC01094 functioned as a molecular sponge for microRNA-577 (miR-577) and consequently enhanced the expression of brain-derived neurotrophic factor (BDNF) in GBM cells. Both miR-577 inhibition and BDNF expression enhancement reversed LINC01094 deficiency-mediated inhibition of malignant processes in GBM cells.