Abstract
ABSTRACT Glioma, one of the most prevalent malignant tumors, is well-known for its poor prognosis and low survival rate among patients. As a type of non-coding RNA, circular RNAs (circRNAs) play a significant role in tumor progression. However, the function and role of circRNAs in glioma development remain unclarified. In our experiments, the relative expression level of circRNA_0067934 and miR-7 in glioma tissue was detected by qRT-PCR, and specific gene knockdown was mediated by siRNA and miRNA-inhibitor. Dual-luciferase reporter assay was carried out to determine whether miR-7 successfully targeted circRNA_0067934. Also, CCK-8 and Transwell were performed to evaluate the malignant behaviors of glioma tissues. Western blotting and immunofluorescence were used to evaluate relative protein expression levels. The results of qRT-PCR indicated that circRNA_0067934 was over-expressed in glioma tissues, and down regulation of circRNA_0067934 reduced the tumor progression by inhibiting cell proliferation, invasion, and migration. The relative expression level of miR-7 was significantly reduced in glioma tissues, which showed a negative association with the expression of circRNA_0067934. CircRNA_0067934 could tagete the miR-7 to regulate progression of glioma cell. In addition, the Wnt/β-catenin signaling pathway might involve in down stream regulation of circRNA_0067934 and miR-7. In conclusion, our results revealed that circRNA_0067934 regulates glioma cells progression by targeting miR-7/ Wnt/β-catenin axis.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.