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Published on: April 10, 2018
Long non-coding RNA SNHG5 promotes glioma progression via miR-205/E2F3 axis
Xiaojian Li1, Liang Liu1, Yidan Luo2
1Department of Neurosurgery, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China.
Abstract:
In recent years, many studies have reported on the abnormal expression and correlation of long non-coding RNAs (lncRNAs) in tumours. However, the accurate molecular mechanism of lncRNAs in glioma is still in its infancy. In the present study, we aimed to explore the molecular mechanism of small nucleolar RNA host gene 5 (SNHG5) in glioma progression. First, we found that SNHG5 expression was higher in glioma and was related to glioma glucose uptake, migration and invasion. Second, through a series of assays, we concluded that SNHG5 acts as a sponge for miR-205, which inhibits tumour growth in glioma by targeting E2F transcription factor 3 (E2F3). Third, using a xenograft mouse model, we demonstrated that SNHG5 regulates tumourigenesis in vivo Taken together, our results show that the SNHG5/miR-205/E2F3 axis is involved in glioma progression and may provide a new therapeutic target for the diagnosis and therapy of glioma.
Insights
Small nucleolar RNA host gene 5 (SNHG5) promotes glioma progression by sponging miR-205 and targeting E2F transcription factor 3 (E2F3). This SNHG5/miR-205/E2F3 axis offers a potential therapeutic target for glioma.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) show abnormal expression in tumors, but their precise mechanisms in glioma are largely unknown.
- Small nucleolar RNA host gene 5 (SNHG5) is implicated in various cancers, yet its role in glioma requires elucidation.
Purpose of the Study:
- To investigate the molecular mechanism of SNHG5 in glioma progression.
- To explore the potential of the SNHG5/miR-205/E2F3 pathway as a therapeutic target for glioma.
Main Methods:
- Quantitative real-time PCR to assess SNHG5 expression in glioma tissues and cell lines.
- Cellular assays to evaluate the impact of SNHG5 on glioma cell glucose uptake, migration, and invasion.
- RNA immunoprecipitation and luciferase reporter assays to confirm the interaction between SNHG5, miR-205, and E2F3.
- Western blotting to detect E2F3 protein levels.
- Xenograft mouse models to validate the role of SNHG5 in glioma tumorigenesis in vivo.
Main Results:
- SNHG5 expression is significantly upregulated in glioma tissues and correlates with increased glucose uptake, migration, and invasion.
- SNHG5 functions as a molecular sponge for miR-205, inhibiting its tumor-suppressive activity.
- miR-205 directly targets E2F transcription factor 3 (E2F3), and SNHG5 overexpression leads to increased E2F3 levels.
- Silencing SNHG5 inhibits glioma tumor growth in vivo.
Conclusions:
- The SNHG5/miR-205/E2F3 axis plays a crucial role in promoting glioma progression.
- Targeting the SNHG5/miR-205/E2F3 pathway presents a promising therapeutic strategy for glioma treatment.
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