Fig. 5

α-catenin stabilizes CEP55 to support HCC cell migration but not proliferation. A Western immunoblot of CEP55 in HLF cells after transfection of two gene-specific siRNAs (#1, #2). Samples were isolated 48 h after transfection. B Cell viability assay of HLF cells after siRNA-mediated silencing of CEP55 at indicated time points. C Proliferation of HLF cells was measured 72 h after siRNA transfection specific for CEP55. D Lateral migration of HLF cells after CEP55 silencing was investigated using a ‘scratch’ assay after 24 h. Cells were pretreated with mitomycin-C to block cell proliferation. E Western immunoblot after inhibition of α‐catenin by siRNAs in HLF cells. Samples were isolated 72 h after transfection. F Real-time PCR analysis of α‐catenin and CEP55 excludes the possibility of transcriptional regulation of CEP55 via an α‐catenin-dependent mechanism. G Lateral migration of HLF cells after CEP55 silencing with and without inducible expression of α‐catenin at indicated time points. Representative pictures of scratches are shown. H Scheme summarizing findings of this study. While the FoxM1/TEAD/YAP complex is required for the overexpression of CEP55, the interaction between α‐catenin and CEP55 is essential for the stabilization of CEP55. CEP55 facilitates a pro-migratory phenotype, likely via activation of the PI3K/AKT pathway and induction of EMT. Additional molecular mechanisms are possible (dashed arrow). Created with BioRender.com (2020), https://app.biorender.com/biorender-templates. Statistical tests in B., C., D., E., G: Mann–Whitney U test. *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001