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Updated: Dec 20, 2025
Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy
Published on: October 4, 2019
MiR-424-5p Inhibits Proliferation, Invasion and Promotes Apoptosis and Predicts Good Prognosis in Glioma by Directly
Zhe Cheng1, Hansheng Shu1, Ying Cui1
1Department of Neurosurgery, The Second Affiliated Hospital of Bengbu Medical College, No. 220 Hongye Road, West of Longzi Lake, Bengbu, Anhui Province, People's Republic of China.
Abstract:
The biological function of miRNA (miR)-424-5p in glioma has not been clarified. This study was to explore the roles of miR-424-5p/Bifunctional apoptosis regulator (BFAR) axis in glioma. Ninety-six pairs of human glioma tissues and their adjacent non-cancer tissues were collected. The levels of BFAR and miR-424-5p were detected by quantitative polymerase chain reaction (qPCR) in glioma tissues and cell lines. Moreover, the biological roles of miR-424-5p and BFAR in glioma cells were assessed. We found a miR-424-5p binding site in the 3'UTR of BFAR by using TargetScan 7.2 online database. The miR-424-5p level was dramatically decreased in glioma tissues and cell lines, and the BFAR expression was significantly increased. The BFAR expression was negatively related to the miR-424-5p level in glioma tissues. Compared to patients with high miR-424-5p levels in glioma tissues, patients with low miR-424-5p levels had significantly lower survival rate (χ2 = 13.728 and P < 0.001). Compared to patients with high BFAR levels in glioma tissues, patients with low BFAR levels had significantly higher survival rate (χ2 = 5.516 and P = 0.027). Furthermore, up-regulation of miR-424-5p obviously restrained glioma cells proliferation and invasion, and promoted apoptosis. Besides, knockdown of BFAR also could markedly inhibit the proliferation and invasion, and promote apoptosis. Finally, overexpression of BFAR in glioma cells partially reversed the inhibited effects of miR-424-5p mimic. Knockdown of miR-424-5p restrained glioma cell apoptosis and promoted invasion and proliferation via regulation of BFAR.
Insights
MicroRNA (miR)-424-5p is decreased in glioma, suppressing tumor growth by targeting Bifunctional apoptosis regulator (BFAR). Restoring miR-424-5p or inhibiting BFAR shows therapeutic potential for glioma.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The role of microRNA (miR)-424-5p in glioma pathogenesis remains unclear.
- Glioma is a primary brain tumor with significant unmet therapeutic needs.
Purpose of the Study:
- To investigate the functional role of the miR-424-5p/Bifunctional apoptosis regulator (BFAR) axis in glioma.
- To determine the prognostic significance of miR-424-5p and BFAR in glioma patients.
Main Methods:
- Quantitative polymerase chain reaction (qPCR) to measure miR-424-5p and BFAR expression in 96 glioma tissues and cell lines.
- Bioinformatic analysis (TargetScan 7.2) to predict miR-424-5p binding sites on BFAR.
- In vitro assays to assess the biological effects of miR-424-5p and BFAR on glioma cell proliferation, invasion, and apoptosis.
Main Results:
- miR-424-5p was significantly downregulated, while BFAR was upregulated in glioma tissues and cell lines.
- BFAR expression was inversely correlated with miR-424-5p levels and associated with poorer patient survival.
- Overexpression of miR-424-5p inhibited glioma cell proliferation and invasion while promoting apoptosis; conversely, BFAR knockdown yielded similar effects.
- BFAR overexpression partially reversed the anti-tumor effects of miR-424-5p mimic.
Conclusions:
- The miR-424-5p/BFAR axis plays a critical role in glioma progression.
- miR-424-5p acts as a tumor suppressor by targeting BFAR, suggesting its potential as a therapeutic target for glioma.
