The levels of circPRELID2, miR-22-3p, and ETS variant 1 (ETV1) were quantified using qRT-PCR. The impact of the circPRELID2/miR-22-3p/ETV1 axis on cell growth, motility, and invasion was evaluated. Protein levels related to this axis were assessed by immunoblotting. The interactions between circPRELID2/miR-22-3p and miR-22-3p/ETV1 were confirmed through RNA immunoprecipitation (RIP), luciferase reporter assays, and RNA pull-down assays.
The results demonstrated that circPRELID2 was upregulated in RCC. Silencing circPRELID2 significantly inhibited RCC cell growth, motility, and invasion.
Additionally, circPRELID2 silencing reduced M2-type macrophage polarisation in THP1-induced macrophage cells. CircPRELID2 was found to sequester miR-22-3p, thereby increasing ETV1 expression through miR-22-3p. The inhibitory effects of circPRELID2 silencing on RCC cell malignancy were mediated through the miR-22-3p/ETV1 axis. Furthermore, in vivo experiments showed that circPRELID2 knockdown hindered the growth of xenograft tumours.
In conclusion, this study demonstrates that silencing circPRELID2 mitigates RCC malignant progression through the circPRELID2/miR-22-3p/ETV1 axis. These findings suggest that targeting circPRELID2 may offer new therapeutic opportunities for the treatment of RCC.
Reference: Lin, X and Zhi, Y. BMC Urol. 2024;24(1):104.
https://doi.org/10.1186/s12894-024-01490-z
Originally Published by Physician’s Weekly. Reused by Medicom Medical Publishers with permission.©2024 Physician’s Weekly. All rights reserved. No works may be reproduced without expressed written consent from Physician’s Weekly. Inquire about licensing here. No article should be construed as medical advice and is not intended as such by the authors or by Physician’s Weekly.
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