Skip to main content
Fig. 4 | Journal of Translational Medicine

Fig. 4

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. 4

P65/FUS promoted FGFR1 transcription. A–C Knockdown of P65 or FUS by siRNAs significantly decreased FGFR1 mRNA and protein levels. D Predicted P65 binding sequence at -609 ~ -619 upstream of transcription start site by analysis with PROMO (https://alggen.lsi.upc.es/cgi-bin/promo_v3/promo/promoinit.cgi?dirDB=TF_8.3) and JASPAR (https://jaspar.genereg.net/). E The predicted P65 binding sequence 5′-GACGTTCCCTA-3′ (in red box) was conserved across species (sequence alignment by UCSC). F Chromatin immunoprecipitation (ChIP) with anti-FUS or anti-P65 showed retrieval of FGFR1 promoter sequences containing the P65 binding site (right panels represented qRT-PCR analysis). Input and nonimmune IgG were used for control. G Dual-luciferase reporter assays showed that FUS or P65 knockdown by siRNAs significantly decreased the FGFR1 promoter activity. Error bars for qRT-PCR, Western blot, ChIP, and Dual-luciferase reporter assays represented mean ± standard deviation (SD) of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001

Back to article page