PD-L1 knockout or ZG16 overexpression inhibits PDAC progression and modulates TAM polarization
CRISPR/Cas9-mediated genome editing has the potential to delete PD-L1 both on the cell surface and inside the cell, thereby inhibiting tumor growth and migration and overcoming immunosuppression. ZG16, with its lectin structure, can reduce PD-L1 expression on the cell surface. However, direct compar...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2025-01-01
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| Series: | Frontiers in Immunology |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2025.1510179/full |
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| Summary: | CRISPR/Cas9-mediated genome editing has the potential to delete PD-L1 both on the cell surface and inside the cell, thereby inhibiting tumor growth and migration and overcoming immunosuppression. ZG16, with its lectin structure, can reduce PD-L1 expression on the cell surface. However, direct comparison of two approaches on PD-L1 expression in Pancreatic ductal adenocarcinoma (PDAC) cells has not yet been investigated. In this study, we established two Panc-1 cell line: one with PD-L1 knockout and another with ZG16 overexpression. Both methods promoted the polarization of tumor-associated macrophages (TAMs) to the M1 phenotype, as indicated by increased levels of the M1 marker CD11c+ in vitro and in vivo. Meanwhile, we observed a reduction in the M2 marker CD206+, upregulation of immune activation-related cytokines/chemokines, and a decrease in immunosuppressive cytokines and tumor angiogenesis factors. In summary, both PD-L1 knockout and ZG16 overexpression represent promising approaches for PDAC treatment. |
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| ISSN: | 1664-3224 |