Abstract
Objective: Wnt/β-catenin pathway upregulation has been correlated with immune evasion in epithelial ovarian cancer. Porcupine (PORCN) enzyme is necessary for cells to produce WNT. Data from our laboratory showed that inhibiting PORCN decreased tumor burden in an ID8 syngeneic ovarian cancer model, which was partially reliant on CD8+ T cells and dendritic cells (DCs). Our objective was to inhibit tumor growth (by knocking out β-catenin in DCs and treating with PORCN inhibitor) in a model resembling high-grade serous ovarian cancer (ID8p53-/-) and investigate changes in the tumor microenvironment (TME).
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