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Updated: Nov 5, 2025

Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy
Published on: October 4, 2019
LINC00511 knockdown suppresses glioma cell malignant progression through miR-15a-5p/AEBP1 axis
Background:
A strong relationship between long intergenic non-protein coding RNA 511 (LINC00511) and glioma has been previously reported but the mechanism of LINC00511 in glioma is yet to be determined. This study examined the mechanism of LINC00511 in glioma.
Methods:
The expression of LINC00511 in glioma was determined by bioinformatics analysis and real-time quantitative PCR (RT-qPCR) analysis. The target relationship between genes was predicted by starBase, TargetScan, and was verified by dual-luciferase. Subsequently, siRNA targeting LINC00511 (siLINC00511) and miR-15a-5p mimic were transfected into glioma cells to examine the effect on biological characteristics using cell counting kit-8, clone formation, flow cytometry, wound-healing, and transwell. MiR-15a-5p inhibitor and AEBP1 were used for in vitro rescue experiments, and tumorigenesis assay and immunohistochemical assays were performed for in vivo experiments. Epithelial-mesenchymal transition (EMT) and p65 phosphorylation were examined by Western blot.
Results:
LINC00511 was predicted and verified to be up-regulated in glioma. SiLINC00511 suppressed cell viability, proliferation, migration and invasion, accelerated apoptosis of glioma cells. Mechanically, siLINC00511 promoted E-cadherin expression but suppressed N-cadherin and Snail expressions. MiR-15a-5p bound to LINC00511, and miR-15a-5p inhibitor partially reversed the effect and regulation of siLINC00511 on glioma cells. AEBP1, a target gene of miR-15a-5p, could activate p65 phosphorylation to promote EMT protein expression and partially reverse the inhibitory effect of miR-15a-5p mimic on the malignant phenotype of glioma cells. SiLINC00511 inhibited tumor growth, down-regulated miR-15a-5p expression and up-regulated AEBP1 and Ki67 expressions in vivo.
Conclusion:
LINC00511 knockdown inhibits glioma cell progression via miR-15a-5p/AEBP1 axis.
Insights
Long intergenic non-protein coding RNA 511 (LINC00511) promotes glioma progression. Knocking down LINC00511 inhibits glioma cell viability, migration, and invasion through the miR-15a-5p/AEBP1 pathway.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- A known association exists between long intergenic non-protein coding RNA 511 (LINC00511) and glioma.
- The precise mechanism by which LINC00511 influences glioma remains unclear.
Purpose of the Study:
- To elucidate the underlying mechanism of LINC00511 in glioma progression.
- To investigate the role of LINC00511 in regulating glioma cell biological characteristics.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) and bioinformatics analyses were used to determine LINC00511 expression in glioma.
- Dual-luciferase assays verified the interaction between LINC00511 and miR-15a-5p.
- In vitro and in vivo experiments, including cell transfection, rescue assays, and tumorigenesis assays, were performed to assess the functional impact of LINC00511 knockdown and the miR-15a-5p/AEBP1 axis.
Main Results:
- LINC00511 was found to be upregulated in glioma tissues.
- LINC00511 knockdown suppressed glioma cell viability, proliferation, migration, invasion, and induced apoptosis.
- The study identified a regulatory axis where LINC00511 influences glioma progression via sponging miR-15a-5p, which targets AEBP1, subsequently affecting p65 phosphorylation and epithelial-mesenchymal transition (EMT).
Conclusions:
- LINC00511 knockdown inhibits glioma cell progression by regulating the miR-15a-5p/AEBP1 axis.
- LINC00511 acts as a potential oncogene in glioma, suggesting therapeutic targeting of this axis.
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