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Characterization of Functionally Associated miRNAs in Glioblastoma and their Engineering into Artificial Clusters for Gene Therapy
Published on: October 4, 2019
SNHG7 Facilitates Glioblastoma Progression by Functioning as a Molecular Sponge for MicroRNA-449b-5p and Thereby
Yaogang Chen1, Shaoyong Yuan1, Tieying Ning1
1Department of Neurosurgery, The Central Hospital of Qingdao, Shandong, China.
Background And Aims:
Long noncoding RNA (small nucleolar RNA host gene 7) has been reported to be involved in multiple malignancies and acts as an oncogene. However, the potential mechanism of small nucleolar RNA host gene 7 in glioblastoma is rarely known. In this study, we attempted to elucidate the biological effects of small nucleolar RNA host gene 7 and the possible molecular mechanism in glioblastoma.
Methods:
The expression level of small nucleolar RNA host gene 7 in glioblastoma tissues and corresponding tumor cell lines was evaluated by using quantitative real-time polymerase chain reaction. Bioinformatics analyses and dual-luciferase reporter gene assay were conducted to verify the correlation among small nucleolar RNA host gene 7, miR-449b-5p, and MYCN. The role of small nucleolar RNA host gene 7 on cell viability, migration, and invasion was measured.
Results:
Small nucleolar RNA host gene 7 expression was markedly increased in glioblastoma tumor tissue. Small nucleolar RNA host gene 7 can sponge miR-449b-5p and negatively regulate miR-449b-5p expression. MiR-449b-5p was remarkably repressed in glioblastoma tissues. Reduction of miR-449b-5p reversed the repressive effects of small nucleolar RNA host gene 7 knockdown on cellular behaviors in glioblastoma. In addition, miR-449b-5p can directly bind with MYCN. Compared with normal samples, MYCN expression was increased. The MYCN expression was negatively related to miR-449b-5p expression while positively related to small nucleolar RNA host gene 7 expression. Rescue experiments revealed that MYCN overexpression reversed the repressive role of small nucleolar RNA host gene 7 knockdown on viability, migration, and invasion of U251 cells.
Conclusion:
In summary, our results demonstrated that small nucleolar RNA host gene 7 regulates glioblastoma proliferation, migration, and invasion via regulating miR-449b-5p and its target gene MYCN, thereby providing a potential therapeutic target for glioblastoma.
Insights
Small nucleolar RNA host gene 7 (SNHG7) promotes glioblastoma growth by inhibiting miR-449b-5p, which targets MYCN. This SNHG7/miR-449b-5p/MYCN axis offers a potential therapeutic strategy for glioblastoma.
Area of Science:
- Molecular Oncology
- Cancer Biology
- RNA Biology
Background:
- Long noncoding RNAs (lncRNAs) are implicated in various cancers.
- Small nucleolar RNA host gene 7 (SNHG7) is an oncogenic lncRNA with poorly understood roles in glioblastoma.
- Investigating SNHG7's mechanism in glioblastoma is crucial for therapeutic development.
Purpose of the Study:
- To elucidate the biological functions of SNHG7 in glioblastoma.
- To identify the molecular mechanism underlying SNHG7's action in glioblastoma.
- To explore SNHG7 as a potential therapeutic target for glioblastoma.
Main Methods:
- Quantitative real-time PCR to assess SNHG7 and miR-449b-5p expression in glioblastoma tissues and cell lines.
- Bioinformatics analysis and dual-luciferase reporter assays to confirm interactions between SNHG7, miR-449b-5p, and MYCN.
- Cell viability, migration, and invasion assays to evaluate SNHG7's functional impact.
Main Results:
- SNHG7 expression is significantly upregulated in glioblastoma tissues.
- SNHG7 acts as a molecular sponge for miR-449b-5p, leading to its repression.
- MiR-449b-5p directly targets MYCN, and their expression levels are inversely correlated with SNHG7 levels.
- Knockdown of SNHG7 inhibits glioblastoma cell proliferation, migration, and invasion, effects reversed by MYCN overexpression.
Conclusions:
- SNHG7 promotes glioblastoma progression by regulating the miR-449b-5p/MYCN axis.
- Targeting the SNHG7/miR-449b-5p/MYCN pathway presents a promising therapeutic avenue for glioblastoma.
- This study provides novel insights into the molecular pathogenesis of glioblastoma.
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