MIR4731 (MicroRNA 4731)

RNA pull down, RIP, dual luciferase reporter assay and expression regulation analysis confirmed the interaction among "circGLIS2-miR-4731-5p-IL-1β" axis. In summary, our findings demonstrated that circGLIS2 facilitated EMs progression by increasing immune cell infiltration via miR-4731-5p/IL-1β axis.

This study reveals that the expression of exosomal miRNA-4731-5p has favorable antitumor properties for the treatment of GBM cell lines and may be a fundamental therapeutic option for this type of brain tumor.

Furthermore, lncRNA PCAT6 modulated notch receptor 3 expression and activated NOTCH signaling pathway via serving as a sponge for miR-4731-5p. Taken together, lncRNA PCAT6 was identified as an oncogene in LSCC, which revealed that PCAT6 might be used as potential therapeutic target for LSCC.

Depleting circPDK1 promotes PTX sensitivity of NSCLC cells via miR-4731-5p/GIGYF1 axis, thereby inhibiting NSCLC pregnancy.

Down-regulation of LINC00466 suppressed the proliferation and arrested the cell cycle of breast cancer cells, and inhibited tumor growth in vivo. LINC00466 promoted BC development via mediating the miR-4731-5p/EPHA2 axis, which has the potential value as a promising therapeutic target in BC.

Our findings underscore the important role of SENCR in regulating the malignant phenotype of AML cells by targeting the miR-4731-5p/IRF2 axis.

Subsequently, results of CCK-8, EdU, Transwell, and aerobic glycolysis detection showed that CCDC183-AS1 plays an oncogene role in BC progression. Furthermore, an investigation of the downstream and upstream factors of CCDC183-AS1 identified a novel MITF/CCDC183-AS1/miR-4731-5p/TCF7L2 axis in BC progression, which might furnish novel insights for developing effective diagnostic and therapeutic strategies for BC.

Rescue experiments showed that miR-4731-5p inhibition and HOXC6 overexpression could reverse the biological behavior of GC cells induced by LINC01857 knockdown. In conclusion, we demonstrated that LINC01857 sponged miR-4731-5p to promote the expression of HOXC6 and eventually acts as an oncogene in GC.

In conclusion, circEHD2 enhances RCC resistance to SU via acting as a miR-4731-5p sponge to mediate ABCF2. MiR-4731-5p can target circEHD2 and ABCF2, thus providing a novel and effective therapeutic against renal cell carcinoma.