Fig. 1: ZBP1 is highly expressed in HNSCC, and its deficiency reduces tumor growth in both orthotopic and chemically induced OSCC mouse models.

A An analysis of ZBP1 expression in HNSC was conducted utilizing the GEPIA2 platform. B, C Expression levels of ZBP1 in HNSCC based on GEO datasets. D A schematic representation of the single-cell RNA sequencing (scRNA-seq) workflow is presented. Tumors derived from Zbp1-deficient and wild-type (WT) mice were dissociated into individual cells, subsequently captured utilizing the 10× Genomics platform, and further processed for library construction and RNA sequencing. E The Orthotopic implantation of MOC-1 cells into the tongues of both Zbp1^−/− and WT mice was performed. F Analysis of body weight alterations in WT and Zbp1^−/− mice bearing tumors following orthotopic implantation of MOC-1 cells. G Evaluation of tumor growth trajectories in WT and Zbp1^−/− mice with orthotopically implanted MOC-1 tumors. H Schematic of the 4NQO-induced OSCC model in WT and Zbp1^−/−mice. I Presentation of representative gross images depicting OSCC progression induced by 4NQO in WT and Zbp1^−/− mice. J Assessment of body weight fluctuations in tumor-bearing WT and Zbp1^−/− mice during the 4NQO-induced OSCC model. K Analysis of tumor growth dynamics in 4NQO-induced OSCC in WT and Zbp1^−/− mice. L Hematoxylin and eosin (H&E) staining of tumor tissues from both the MOC-1 orthotopic model and the 4NQO-induced model in WT and Zbp1^−/− mice. M Immunohistochemical analysis of Ki-67 and β-catenin expression in tumors derived from MOC-1 orthotopic implantation in WT and Zbp1^−/−mice.