Fig. 3

FER1L4 sponged miR-92a-3p in prostate cancer cells. a RegRNA 2.0 software predicted the potential binding site and secondary structure of FER1L4/miR-92a-3p interaction. b Analysis of TCGA-PRAD showed that miR-92a-3p was overexpressed in prostate cancer tissues (n = 495) compared with normal prostate tissues (n = 52). c RT-qPCR was applied to detect miR-92a-3p expression in 78 pairs of tumors and normal tissues. Pearson correlation analysis indicated a strong negative correlation between miR-92a-3p and FER1L4 expression. d, e RT-qPCR showed that overexpression of FER1L4 decreased miR-92a-3p expression in PC-3 (d) and DU145 (e) cells. f, g RT-qPCR showed that transfection of miR-92a-3p inhibitor decreased miR-92a-3p expression in PC-3 (f) and DU145 (g) cells. H-I. RT-qPCR showed that decreased expression of miR-92a-3p elevated FER1L4 expression in PC-3 (h) and DU145 cells (i). j, k RT-qPCR showed that transfection of miR-92a-3p mimic increased miR-92a-3p expression in PC-3 (j) and DU145 cells (k). l, m The dual luciferase reporter assay was applied to analyze the direct binding between miR-92a-3p and FER1L4. Overexpression of miR-92a-3p reduced relative luciferase activity of pGL3-FER1L4-WT in PC-3 (l) and DU145 cells (m). n In the RNA pull down assay, RT-qPCR was performed to analyze the enrichment of FERL14 by Bio-NC probe, Bio-miR-92a-3p-WT and Bio-miR-92a-3p-Mut. ***p < 0.001