Fig. 7

RBAT1 recruits HNRNPL to activate E2F3 expression. a Schematic diagram of ChIP assay sites in E2F3 promoter region. P1-P5: primer names; gray arrow: E2F3 promoter region (1000 bp upstream from TSS; P3-P4, P5-P6: different ChIP sites of E2F3 promoter); red arrow: transcriptional direction; blue box: exons of the E2F3 gene. b-c Real-time PCR showing the interaction of HNRNPL with E2F3 promoter in tumor cell lines (Y79, WERI-Rb-1 and 5637) compared with ARPE-19 and SV-HUC-1 from ChIP assay. IgG: negative control. The results are shown as the mean ± SD. NS means no significant difference, ** p < 0.01. d ChIP analysis showed that the depletion of either RBAT1 or HNRNPL decreases the enrichment of HNRNPL at E2F3 promoter. The knockdown efficiency of shHNRNPL-1 was verified by western blotting, and RBAT1 knockdown did not influence the expression level of HNRNPL. IgG: negative control. e Verified E2F3 promoter sequences (− 500 to − 1000 bp) were constructed into a pGL3 vector and subjected to luciferase reporter assays in either RBAT1- or HNRNPL-silenced tumor cell lines (Y79, WERI-Rb-1 and 5637). Mock: negative control group transfected with empty pGL3 vector; Ctrl: negative control group transfected with scrambled GapmeR. The results are shown as the mean ± SD, *p < 0.05 and **p < 0.01