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The following is a summary of “Role of MUC16 in tumor biology and tumor immunology in ovarian cancer,” published in the February 2025 issue of the BMC Cancer by Yang et al.

This study investigates the role of glycoproteomic alterations, particularly MUC16, in modulating NK cell-mediated immunotherapy response in ovarian cancer. By analyzing glycoprotein expression profiles from the CPTAC database, MUC16 was identified as significantly upregulated in ovarian cancer tissues, correlating with increased tumor invasiveness and immune evasion. Functional experiments revealed that MUC16 knockdown enhanced NK cell cytotoxicity, reduced tumor invasiveness, and promoted NK cell activation, whereas MUC16 overexpression resulted in the opposite effects. 

In vivo models further demonstrated that silencing MUC16 led to suppressed tumor growth, increased NK cell infiltration into the tumor microenvironment, and enhanced NK cell activation, reinforcing the role of MUC16 in immune resistance mechanisms. These findings highlight MUC16 as a crucial regulator of NK cell-mediated immune responses and suggest that targeting MUC16 could be a promising strategy to improve immunotherapeutic efficacy in ovarian cancer. Future research should explore therapeutic interventions aimed at modulating MUC16 expression to enhance immune system engagement and overcome resistance to NK cell-based therapies.

Source: bmccancer.biomedcentral.com/articles/10.1186/s12885-025-13461-0