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.
Keywords: EMX2OS; Wilms’ tumor; lncRNA; miR-654-3p.
© 2022 by the Association of Clinical Scientists, Inc.