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Fig. 8 | Journal of Translational Medicine

Fig. 8

From: A novel intronic circular RNA circFGFR1int2 up-regulates FGFR1 by recruiting transcriptional activators P65/FUS and suppressing miR-4687-5p to promote prostate cancer progression

Fig. 8

CircFGFR1int2 suppressed the inhibitory effects of miR-4687-5p on FGFR1. A Artificial overexpression of miR-4687-5p by miR-4687-5p mimic significantly decreased expressions of FGFR1 mRNA and protein in PCa cells, which could be reversed by circFGFR1int2 artificial overexpression (OE-circFGFR1int2). B CircFGFR1int2 and miR-4687-5p were simultaneously precipitated by anti-AGO2 in PCa cells. Artificial overexpression of miR-4687-5p or knockdown of circFGFR1int2 decreased the recovery of circFGFR1int2. C Artificial overexpression of miR-4687-5p increased AGO2 pull down by biotin-labeled miR-4687-5p probe, whereas knockdown of circFGFR1int2 decreased AGO2 retrieval. D Artificial overexpression of miR-4687-5p mimic significantly suppressed the promoter activity of the WT constructs containing the miR-4687-5p binding sited (pGL3-FGFR1 3′UTR-WT, pMIR-FGFR1 CDS-WT, and pGL3-circFGFR1int2-WT), which could be rescued by the respective mutant plasmids (pGL3-FGFR1 3′UTR-MUT, pMIR-FGFR1 CDS-MUT and pGL3-circFGFR1int2-MUT). Error bars for qRT-PCR and Dual-luciferase reporter assays represented mean ± standard deviation (SD) of three independent experiments. **P < 0.01, ***P < 0.001

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