Fig. 2: USP1 depletion inhibits Hippo/TAZ axis activity in HCC cells.

A, E, I Western blot analysis of USP1 and TAZ expression in HLF, Hep3B, and HEK293 cells exposed as indicated. In this study, actin was employed as an internal reference. B, F, J RT–qPCR results of TAZ mRNA expression in HLF, Hep3B, and HEK293 cell lines exposed as indicated. C, G, K RT–qPCR results of CTGF and CYR61 mRNA expression in HLF, Hep3B, and HEK293 cell lines exposed as indicated. D, H, L In HLF, Hep3B, and HEK293 cells exposed as indicated, transcriptional activity of TEAD response elements was measured by a luciferase assay using a reporter containing tandem TEAD-binding sites. M In the TCGA database, the relative level of TAZ RNA in HCC tumor samples (n = 371) was compared to that in normal samples (n = 50) (https://www.genome.gov/). N In HCC tumors of various stages (Stag I, n = 168; Stag II, n = 84; Stag III, n = 82; Stag IV, n = 6), the relative RNA level of TAZ was compared with that in normal liver tissue (n = 50). Data were obtained from the TCGA database. (https://www.genome.gov/). O Comparing with lower TAZ expression (n = 275), higher TAZ expression (n = 90) was associated with poorer progression-free survival in HCC patients based on Kaplan‒Meier analysis in TCGA. P = 0.00044, log-rank test. P, Q Immunohistochemical (IHC) staining to evaluate USP1 and TAZ expression in HCC tissues. In Panels A–L the results are representative of three independent experiments. All the data are presented as the means ± SDs. **P < 0.01, ***P < 0.001 (Student’s t test).