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Programmed cell death ligand 1 ( PD ‐L1) on tumor cells suppresses anti‐tumor immunity and has an unfavorable prognostic impact in ovarian cancer patients. We herein report the pathophysiological and therapeutic impacts of  PD ‐L1 disruption in ovarian cancer.  PD ‐L1 was genetically disrupted in the murine ovarian cancer cell line  ID 8 using clustered regularly interspaced short palindromic repeats ( CRISPR )/Cas9‐mediated genome editing.  PD ‐L1 knockout ( KO ) and control ovarian cancer cells were intraperitoneally inoculated into syngeneic mice, and survival and tumor dissemination were evaluated. Survival times were significantly longer in the  PD ‐L1‐ KO ID 8‐inoculated groups than in their control groups, and its therapeutic benefit was enhanced in combination with the cisplatin treatment. Tumor weights and ascites volumes were significantly lower in the  PD ‐L1‐ KO ID 8 groups than in their control groups. Immunohistochemical and immunofluorescence analyses showed that intratumoral  CD 4 +  T cells,  CD 8 +  T cells,  NK  cells and  CD 11c +  M1 macrophages were significantly increased, whereas regulatory T cells were significantly decreased in the  PD ‐L1‐ KO ID 8 groups compared with those in their control groups. The intratumoral  mRNA  expression of interferon‐γ, tumor‐necrosis factor‐α, interleukin ( IL )‐2,  IL ‐12a,  CXCL 9 and  CXCL 10 was significantly stronger, while that of  IL ‐10, vascular endothelial growth factor,  CXCL 1 and  CXCL 2 was significantly weaker in the  PD ‐L1‐ KO ID 8 groups. These results indicate that  CRISPR /Cas9‐mediated  PD ‐L1 disruption on tumor cells promotes anti‐tumor immunity by increasing tumor‐infiltrating lymphocytes and modulating cytokine/chemokine profiles within the tumor microenvironment, thereby suppressing ovarian cancer progression. These results suggest that  PD ‐L1‐targeted therapy by genome editing may be a novel therapeutic strategy for ovarian cancer.

cancer science

Programmed cell death ligand 1  d isruption by  clustered regularly interspaced short palindromic repeats /Cas9‐genome editing promotes antitumor immunity and suppresses ovarian cancer progression