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UPF1 alleviates the progression of glioma via targeting lncRNA CYTOR
1Department of Neurosurgery, The First Affiliated Hospital, Nanchang University, Nanchang, China. xujiang81@163.com.
Objective:
To uncover the role of UPF1 in alleviating the progression of glioma via targeting long non-coding RNA (lncRNA) CYTOR and underlying mechanism.
Patients And Methods:
A total of 30 glioma tissues surgically resected from glioma patients and 30 brain tissues were collected from brain trauma patients undergoing craniotomy during the same period. Relative levels of UPF1 and CYTOR in collected tissues were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Correlation between levels of UPF1 and CYTOR in glioma tissues was assessed, and the regulatory effects of UPF1/CYTOR on proliferative and invasive abilities in U87 and LN229 cells were evaluated by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) and transwell assay, respectively. In addition, the interaction between UPF1 and CYTOR was explored by RIP (RNA-Binding Protein Immunoprecipitation) assay. Through Actinomycin D treatment in U87 and LN229 cells, RNA stability of CYTOR influenced by UPF1 was determined. Finally, rescue experiments were conducted to ascertain the involvement of CYTOR in UPF1-regulated progression of glioma.
Results:
UPF1 was downregulated in glioma tissues and cells. A lower level of UPF1 was observed in glioma tissues in the more advanced stage with a larger tumor size. Besides, the overexpression of UPF1 markedly suppressed proliferation and invasion abilities of U87 and LN229 cells, and CYTOR was upregulated in glioma tissues and cells, which was negatively correlated with UPF1 level. Moreover, the overexpression of UPF1 decreased the half-life of CYTOR in glioma cells. Furthermore, the RIP assay confirmed the interaction between UPF1 and CYTOR. Rescue experiments finally confirmed that the overexpression of CYTOR partially reversed the inhibitory effects of UPF1 on proliferation and invasion abilities in glioma.
Conclusions:
UPF1 is down-regulated in glioma and alleviates the progression of glioma via targeting CYTOR.
Insights
The study found that UPF1 is downregulated in glioma, suppressing tumor progression by targeting the long non-coding RNA CYTOR. Restoring UPF1 levels inhibits glioma cell proliferation and invasion.
Area of Science:
- Neuro-oncology
- Molecular Biology
- RNA Biology
Background:
- Glioma is a primary brain tumor with significant morbidity and mortality.
- Understanding the molecular mechanisms underlying glioma progression is crucial for developing effective therapies.
- The role of specific RNA-binding proteins and long non-coding RNAs in glioma remains an active area of research.
Purpose of the Study:
- To investigate the role of UPF1 in glioma progression.
- To determine if UPF1 targets the long non-coding RNA (lncRNA) CYTOR.
- To elucidate the underlying molecular mechanisms of UPF1-mediated glioma regulation.
Main Methods:
- Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) to measure UPF1 and CYTOR levels in glioma and normal brain tissues.
- Cell proliferation and invasion assays (MTT and transwell) to assess the functional impact of UPF1 and CYTOR.
- RNA-Binding Protein Immunoprecipitation (RIP) assay to confirm UPF1-CYTOR interaction.
- Actinomycin D treatment to determine RNA stability.
- Rescue experiments to validate the role of CYTOR in UPF1-regulated glioma progression.
Main Results:
- UPF1 expression was significantly downregulated in glioma tissues and cells, correlating with advanced tumor stage and size.
- Overexpression of UPF1 suppressed glioma cell proliferation and invasion.
- CYTOR was upregulated in glioma and negatively correlated with UPF1 levels.
- UPF1 overexpression reduced CYTOR stability, and RIP assays confirmed their interaction.
- Overexpression of CYTOR partially reversed the inhibitory effects of UPF1.
Conclusions:
- UPF1 acts as a tumor suppressor in glioma.
- UPF1 alleviates glioma progression by targeting and destabilizing the lncRNA CYTOR.
- These findings identify a novel UPF1-CYTOR regulatory axis in glioma pathogenesis.