Fig. 6: Targeting USP5 potentiates anti-PD-L1 immunotherapy in murine HCC models.

a Tumor growth of sgCtrl and sgUsp5 Hepa1-6 cells in C57BL/6 mice with anti-IgG mAb or anti-PD-L1 mAb treatments. n = 10. b Kaplan-Meier survival curves for four treatment groups demonstrate the improved efficacy of PD-L1 mAb after knockout Usp5. **P < 0.01. c A schematic model illustrating the treatment plan for mice bearing subcutaneous Hepa1-6 or H22 tumors. Male C57BL/6 mice were implanted with Hepa1-6 or H22 cells subcutaneously and treated with four arms: control antibody (anti-IgG mAb) treatment, anti-PD-L1 mAb treatment, USP5 inhibitor WP1130 treatment, and anti-PD-L1 mAb plus USP5 inhibitor combination treatment. d Hepa1-6 and H22 implanted tumor-bearing mice were enrolled in different treatment groups as indicated. Tumor volumes of mice treated with control antibody, anti-PD-L1 mAb, the USP5 inhibitor WP1130, or combined therapy were measured every 3 days and plotted individually. n = 10 mice per group. e Kaplan-Meier survival curves for each treatment group demonstrate the improved efficacy of combining PD-L1 mAb with the USP5 inhibitor WP1130. *** P < 0.001. f Immunohistochemical (IHC) analysis of Cd8, Granzyme B (GzmB), Tim-3, Ythdf1 and Pd-l1 expression in Hepa1-6 tumors after indicated treatments. g Representative multiplex immunohistochemistry (mIHC) images of Cd8 (Gray), GzmB (Green), Tim-3 (Red), and DAPI nuclear staining (blue) in Hepa1-6 tumors after indicated treatments. All data are presented as mean ± SEM. Source data are provided as a Source Data file.