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Knockdown of Long Non-Coding RNA KCNQ1OT1 Restrained Glioma Cells' Malignancy by Activating miR-370/CCNE2 Axis
Wei Gong1, Jian Zheng2, Xiaobai Liu2
1Department of Neurobiology, College of Basic Medicine, China Medical UniversityShenyang, China; Key Laboratory of Cell Biology, Ministry of Public Health of China, Key Laboratory of Medical Cell Biology, Ministry of Education of China, China Medical UniversityShenyang, China.
Abstract:
Accumulating evidence has highlighted the potential role of long non-coding RNAs (lncRNAs) as biomarkers and therapeutic targets in solid tumors. Here, we elucidated the function and possible molecular mechanisms of lncRNA KCNQ1OT1 in human glioma U87 and U251 cells. Quantitative Real-Time polymerase chain reaction (qRT-PCR) demonstrated that KCNQ1OT1 expression was up-regulated in glioma tissues and cells. Knockdown of KCNQ1OT1 exerted tumor-suppressive function in glioma cells. Moreover, a binding region was confirmed between KCNQ1OT1 and miR-370 by dual-luciferase assays. qRT-PCR showed that miR-370 was down-regulated in human glioma tissue and cells. In addition, restoration of miR-370 exerted tumor-suppressive function via inhibiting cell proliferation, migration and invasion, while promoting the apoptosis of human glioma cells. Knockdown of KCNQ1OT1 decreased the expression level of Cyclin E2 (CCNE2) by binding to miR-370. Further, miR-370 bound to CCNE2 3'UTR region and decreased the expression of CCNE2. These results provided a comprehensive analysis of KCNQ1OT1-miR-370-CCNE2 axis in human glioma cells and might provide a novel strategy for glioma treatment.
Insights
Long non-coding RNA KCNQ1OT1 promotes glioma progression by downregulating miR-370, which targets CCNE2. Inhibiting KCNQ1OT1 may offer a novel therapeutic strategy for glioma treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in solid tumors, serving as potential biomarkers and therapeutic targets.
- Glioma, a primary brain tumor, presents significant challenges in treatment, necessitating the identification of novel therapeutic strategies.
Purpose of the Study:
- To investigate the function and molecular mechanisms of lncRNA KCNQ1OT1 in human glioma cells.
- To elucidate the regulatory axis involving KCNQ1OT1, miR-370, and CCNE2 in glioma progression.
Main Methods:
- Quantitative Real-Time polymerase chain reaction (qRT-PCR) to assess gene expression levels.
- Dual-luciferase reporter assays to confirm binding interactions between KCNQ1OT1 and miR-370.
- Cell proliferation, migration, invasion, and apoptosis assays to evaluate functional effects.
Main Results:
- KCNQ1OT1 expression was significantly upregulated in glioma tissues and cells.
- Knockdown of KCNQ1OT1 exhibited tumor-suppressive effects in glioma cells.
- KCNQ1OT1 directly binds to miR-370, leading to its downregulation. MiR-370 restoration suppressed proliferation, migration, and invasion while promoting apoptosis.
- KCNQ1OT1 knockdown reduced CCNE2 expression via miR-370, and miR-370 directly targeted CCNE2, decreasing its expression.
Conclusions:
- The KCNQ1OT1/miR-370/CCNE2 axis plays a crucial role in human glioma progression.
- KCNQ1OT1 acts as an oncogenic lncRNA in glioma by sponging miR-370 and subsequently upregulating CCNE2.
- Targeting the KCNQ1OT1-miR-370-CCNE2 pathway presents a promising novel therapeutic strategy for glioma.