Skip to main content
Fig. 9 | Journal of Experimental & Clinical Cancer Research

Fig. 9

From: HNRNPL induced circFAM13B increased bladder cancer immunotherapy sensitivity via inhibiting glycolysis through IGF2BP1/PKM2 pathway

Fig. 9

HNRNPL induced the back-splicing of circFAM13B. A RNA–protein pulldown experiment and silver staining assay were conducted to investigate the possible proteins, which could bind the flanking introns of circFAM13B. B Mass spectrometry assay results indicated that HNRNPL was pulled down by the probes of flanking introns of circFAM13B. C The binding sites of HNRNPL in the flanking introns sequences of the pre-FAM13B mRNA were predicted via catRAPID. D RNA–protein pulldown and Western blot assays were performed to confirm that the flanking introns of circFAM13B could bind to HNRNPL. E RIP assay in T24 cells was conducted to validate the binding of HNRNPL and flanking introns of circFAM13B (**P < 0.01, Student’s t-test). F IF-FISH assays were carried out to indicate the co-localisation of circFAM13B and HNRNPL in T24 cells. G QRT-PCR assays were performed to validate the expression level of circFAM13B in HNRNPL knockdown T24 and UMUC3 cells (**P < 0.01, ***P < 0.001, Student’s t-test). H Pearson’s correlation analysis was conducted to validate the correlation of circFAM13B and HNRNPL. Data are expressed as mean ± SD, n = 3

Back to article page