PTK7 enrichment in HCC tumor is not driven by and does not result in the activation of Wnt signaling. (A) A bioinformatic analysis was performed on TCGA-LIHC cohort to compare the transcriptomic level of PTK7 under HCC driven by different CTNNB1 status. Groups were compared by Student t test. (B) IHC was performed on formalin-fixed, paraffin-embedded tissue of terminal livers dissected from C57BL/6 mice transformed with a ΔN90-CTNNB1/c-MYC driver plasmid by hydrodynamic tail-vein injection. Representative IHC images showing PTK7 and β-catenin expression pattern at tumor boundaries. (C) The subcellular localization of β-catenin was investigated in MHCC97L cells overexpressing PTK7 by subcellular fractionation and Western blot. (D) The transcriptional activity of β-catenin in Wnt3a-stimulated MHCC97L cells overexpressing PTK7 was examined by TOP/FOP assay and compared with treated EV control by Student t test. NOT, nontumor; OE, overexpression; T, tumor. P values (∗P < .05, ∗∗P < .01, ∗∗∗P < .001).