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Updated: Dec 14, 2025
Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy
Published on: October 4, 2019
Knockdown of long non-coding RNA LINC00467 inhibits glioma cell progression via modulation of E2F3 targeted by
Shuzi Gao1, Haixia Duan2, Dezhu An3
1Department of Cerebrovascular Diseases, Zhuhai People's Hospital (Zhuhai Hospital Affiliated with Jinan University) , Zhuhai City, Guangdong Province, PR. China.
Abstract:
Studies have found that LINC00467 is an important regulator of cancer. However, the function of LINC00467 in glioma cell is unclear. Therefore, this experimental design based on LINC00467 to explore its mechanism of action in glioma cell. RT-qPCR was used to detect the expression of LINC0046 and miR-200a in glioma cell lines. MTT assay, Edru assay and Transwell assay and flow cytometry were used to detect the effects of LINC0046 and miR-200a on PC cell proliferation, migration and apoptosis. Target gene prediction and screening, luciferase reporter assays were used to validate downstream target genes for LINC0046 and miR-200a. Western blotting was used to detect the protein expression of E2F3. The tumor changes in mice were detected by in vivo experiments in nude mice. LINC00467 was up-regulated in glioma cells. Knockdown of LINC00467 inhibited the viability, migration and invasion of glioma cells. In glioma cells, miR-200a was significantly reduced, while E2F3 was significantly rised. LINC00467 negatively regulated the expression of miR-200a in gliomas, while miR-200a negatively regulated the expression of E2F3 in gliomas. INC00467 promoted the development of glioma by inhibiting miR-200a and promoting E2F3 expression. LINC00467 may be a potential therapeutic target for gliomas.
Insights
Long non-coding RNA LINC00467 promotes glioma development by suppressing miR-200a and increasing E2F3. This study reveals LINC00467 as a potential therapeutic target for glioma treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in cancer.
- The specific function of LINC00467 in glioma, a primary brain tumor, remains largely unelucidated.
- Understanding lncRNA mechanisms is crucial for developing novel cancer therapies.
Purpose of the Study:
- To investigate the functional role and molecular mechanism of LINC00467 in glioma cells.
- To determine the regulatory relationship between LINC00467, miR-200a, and E2F3 in glioma.
- To assess the therapeutic potential of targeting LINC00467 in glioma.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) for gene expression analysis.
- Cell viability (MTT), proliferation (EdU), migration, invasion (Transwell), and apoptosis assays.
- Bioinformatic prediction, luciferase reporter assays for target validation, and Western blotting for protein analysis.
- In vivo tumor xenograft models in nude mice.
Main Results:
- LINC00467 expression was significantly upregulated in glioma cells.
- Knockdown of LINC00467 inhibited glioma cell proliferation, migration, and invasion.
- LINC00467 negatively regulated miR-200a and positively regulated E2F3 expression, promoting glioma progression.
- In vivo experiments confirmed LINC00467's role in promoting tumor growth.
Conclusions:
- LINC00467 promotes glioma development by inhibiting miR-200a and upregulating E2F3.
- The LINC00467/miR-200a/E2F3 axis represents a novel regulatory pathway in glioma.
- LINC00467 emerges as a promising therapeutic target for glioma treatment.
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