Fig. 4

The TEADs/FoxM1/YAP complex regulates CEP55 overexpression in liver cancer cells. A CEP55 transcriptome data derived from human HCC tissues and adjacent liver tissues are compared [23]. Statistical test: Mann–Whitney U test. ***p ≤ 0.001. B Kaplan–Meier plots of HCC patients showing overall survival and cancer recurrence depending on CEP55 expression. Patients were divided in groups with low and high CEP55 expression using Cutoff Finder. Statistical test: log-rank test. p-values and group sizes are indicated. C Scheme depicting ChIP-Seq profiles in the promoter region of the human CEP55 gene. Data for FoxM1, TEAD4, and YAP are shown. The TEAD/YAP target gene CTGF is shown as positive control. Binding sites for TEAD4 and FoxM1 in the promoter of CEP55 were selected using the JASPAR database. D Western Immunoblot data of HLF cells after gene-specific silencing of TEAD1/3/4 family members, FoxM1, and YAP for 48 h. Due to structural differences, TEAD2 is not efficiently targeted by the chosen siRNAs. E–G Real-time PCR analysis of TEAD1-4 and CEP55 (E), FoxM1 and CEP55 (F), as well as YAP and CEP55 (G) after silencing of the respective transcriptional regulator. Analysis was performed using HLF cells. Statistical test: Mann–Whitney U test. **p ≤ 0.01, ***p ≤ 0.001. H-J ChIP analysis of TEAD4 (H), FoxM1 (I), and YAP (J) at two predicted binding sites (BS) in the CEP55 promoter (BS#1 and BS#2). Two CEP55 upstream promoter regions served as negative controls (BS#1 and BS#2). IgG was employed as antibody control. Results were normalized to respective IgG controls. Western blots in H-J illustrate successful IP of TEADs, FoxM1, and YAP