Photo Credit: Alena Butusava
The following is a summary of “CircPRELID2 functions as a promoter of renal cell carcinoma through the miR-22-3p/ETV1 cascade,” published in the May 2024 issue of Urology by Lin et al.
Emerging evidence has highlighted the involvement of circular RNAs (circRNAs) in renal cell carcinoma (RCC) carcinogenesis. However, the specific role and molecular mechanisms of circPRELID2 (hsa_circ_0006528) in RCC progression remain unclear. This study aimed to elucidate the function of circPRELID2 in RCC.
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 polarization 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 tumors.
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.
Source: bmcurol.biomedcentral.com/articles/10.1186/s12894-024-01490-z
