This study investigates the role of centrosomal protein CEP55 in immune evasion by liver cancer cells and evaluates the effects of its knockout using CRISPR-Cas9 technology. CEP55-knockout models were established in human hepatocellular carcinoma cell lines Huh7 and HepG2, and alterations in immune-related molecules, tumor cell behavior, and antitumor immune responses were systematically assessed. CEP55 knockout significantly reduced PD-L1 expression while upregulating MHC class I levels, thereby enhancing tumor immunogenicity. Mechanistically, CEP55 deletion attenuated STAT1 activation, particularly under interferon-γ (IFN-γ) stimulation, suggesting involvement of the IFN-γ-STAT1 signaling axis in CEP55-mediated immune regulation. In parallel, CEP55 knockout markedly decreased intracellular reactive oxygen species (ROS) levels and suppressed the secretion of immunosuppressive cytokines IL-10 and TGF-β, indicating remodeling of the immunosuppressive tumor microenvironment. Functional assays demonstrated that CEP55 deficiency inhibited tumor cell migration and invasion and promoted apoptosis. Importantly, co-culture experiments revealed that CEP55 knockout enhanced T cell effector function, as evidenced by increased secretion of IFN-γ and Granzyme B and restored T cell-mediated cytotoxicity, even in the presence of IFN-γ stimulation. Collectively, these findings indicate that CEP55 promotes liver cancer immune escape and malignant progression through modulation of STAT1-dependent PD-L1/MHC-I expression, oxidative stress, and immunosuppressive signaling. Targeting CEP55 may therefore represent a potential strategy to improve antitumor immune recognition in liver cancer.
Keywords: CEP55; CRISPR-Cas9; Immune escape; Liver cancer; PD-L1.
© 2026. The Author(s).