Fig. 1: SP1 is a coregulator of TEAD4 in CRC.
A GSEA revealed significant enrichment of conserved YAP target genes in SP1-knockdown HCT116 cells. B Heatmap showing the mRNA levels of SP1 and Hippo target genes in HCT116 cells with SP1 knockdown, as detected by qPCR. The Z score of each sample was calculated and is shown as a heatmap. C Motif enrichment analysis of the TEAD4 binding sites in HCT116 cells. D Heatmaps of ChIP-seq data for SP1 and TEAD4 in HCT116 cells. E Normalized read density for SP1 and TEAD4 is plotted in the region ±2.0 kb from the TEAD4 peak center. F Venn diagram displaying the overlap between the SP1 and TEAD4 target genes in HCT116 cells. A hypergeometric test was performed to calculate the statistical significance. G Genome browser view of TEAD4 (red) and SP1 (green) ChIP-seq tracks at the CTGF/CYR61/AMOTL2 loci in HCT116 cells. H ChIP‒qPCR analysis of SP1 binding at the CTGF/CYR61/ANKRD1 locus in HCT116 cells. I A luciferase reporter assay revealed that SP1 was a positive regulator of YAP/TAZ activity. HEK293T cells were transiently transfected with the indicated plasmids and a TEAD-luciferase reporter. J Transwell assays of YAP5SA-overexpressing HCT116 cells with SP1 knockdown. K Representative images of xenograft tumors derived from YAP5SA-overexpressing HCT116 cells with SP1 knockdown are shown.
