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Published on: April 7, 2017
EMX2OS Delays Wilms'Tumor Progression via Targeting miR-654-3p
Zhi-Hong Chen1, Ming-Yu Cui2, Hong-Mei Zhang3
1Department of Urology, Qilu Children's Hospital of Shandong University, Jinan, Shandong, China.
Objective:
Wilms' tumor is the most common renal cancer among children, and a number of patients with high-risk histology still have a poor prognosis. This study explored the biological function and its potential mechanisms of lncRNA EMX2 opposite strand/antisense RNA (EMX2OS) in the progression of Wilms' tumor.
Materials:
Expression of EMX2OS and miR-654-3p was assessed by RT-qPCR. CCK-8 assay was adopted to assess Wilms' tumor cell proliferation. Apoptosis was determined by Annexin V/PI staining. Transwell assay was utilized to detect the migratory and invasive abilities. The interaction between miR-654-3p and EMX2OS was confirmed by dual luciferase assay. The protein levels of apoptosis-related proteins were detected by Western blotting. Xenograft transplantation was carried out to evaluate tumor growth in vivo.
Results:
EMX2OS expression was lower, while miR-654-3p level was higher in Wilms' tumor patient samples, and there was a negative correlation between EMX2OS and miR-654-3p. Overexpression of EMX2OS repressed growth, migration, invasion, and triggered apoptosis of Wilms' tumor cells. EMX2OS acted as a sponge of miR-654-3p. Overexpression of miR-654-3p abolished EMX2OS-mediated anti-cancer effects on Wilms' tumor cells. Finally, EMX2OS overexpression restrained Wilms' tumor growth in vivo.
Conclusion:
EMX2OS slowed down the progression of Wilms' tumor via targeting miR-654-3p, which provided evidence for the conclusion that EMX2OS may be a novel therapeutic target for Wilms' tumor.
Insights
Long non-coding RNA EMX2 opposite strand/antisense RNA (EMX2OS) inhibits Wilms' tumor progression by targeting microRNA-654-3p. EMX2OS may serve as a novel therapeutic target for this pediatric renal cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Wilms' tumor is the most common pediatric renal cancer.
- High-risk Wilms' tumor patients often have a poor prognosis.
- Understanding the molecular mechanisms driving Wilms' tumor progression is crucial for developing effective therapies.
Purpose of the Study:
- To investigate the biological function of lncRNA EMX2 opposite strand/antisense RNA (EMX2OS) in Wilms' tumor.
- To elucidate the potential mechanisms underlying EMX2OS's role in Wilms' tumor progression.
- To explore EMX2OS as a potential therapeutic target for Wilms' tumor.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) to assess EMX2OS and miR-654-3p expression.
- Cell Counting Kit-8 (CCK-8) assay for proliferation, Annexin V/PI staining for apoptosis, and Transwell assay for migration and invasion.
- Dual luciferase assay to confirm interaction, Western blotting for protein analysis, and in vivo xenograft transplantation studies.
Main Results:
- EMX2OS expression was downregulated, while miR-654-3p was upregulated in Wilms' tumor samples, showing a negative correlation.
- EMX2OS overexpression suppressed Wilms' tumor cell growth, migration, and invasion, while promoting apoptosis.
- EMX2OS functioned as a molecular sponge for miR-654-3p, and miR-654-3p overexpression reversed EMX2OS-mediated anti-cancer effects. EMX2OS inhibited tumor growth in vivo.
Conclusions:
- EMX2OS significantly inhibits Wilms' tumor progression by targeting miR-654-3p.
- EMX2OS demonstrates potential as a novel therapeutic target for Wilms' tumor.
- This study provides critical insights into the molecular underpinnings of Wilms' tumor and potential therapeutic strategies.
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