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• W4294132531 abstract "Programmed death ligand 1 (PD-L1) is widely known as an immune checkpoint, and immunotherapy through the inhibition of checkpoint molecules has become an important component in the successful treatment of tumours via programmed death 1 (PD-1)/PD-L1 signalling pathways. However, its biological functions and expression profile in colorectal cancer (CRC) are elusive. We previously found that PD-L1 can bind to PD-L1 and cause cell detachment. However, the detailed molecular mechanisms of how PD-L1 binds to PD-L1 and how it transmits signals to the cell remain unclear. In this study, we disclosed that PD-L1 expression was dramatically upregulated in CRC compared to normal tissues. Ectopic expression of PD-L1 inhibits cell adhesive capacity and promotes cell migration in CRC cell lines, while silencing PD-L1 had the opposite effects and suppressed invasion and proliferation. Mechanistically, PD-L1 was found to promote epithelial-mesenchymal transition (EMT) through the ERK signalling molecule pathway and interacted with the 1-86 aa fragment of KRAS to transduce signals. Collectively, our study demonstrated the role of PD-L1 after binding to PD-L1 in CRC, thereby providing a new theoretical basis for further improving immunotherapy with anti-PD-L1 antibodies." @default.
• W4294132531 created "2022-09-02" @default.
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• W4294132531 date "2022-09-15" @default.
• W4294132531 modified "2023-09-25" @default.
• W4294132531 title "<scp>PD‐L1</scp>/<scp>PD‐L1</scp> signalling promotes colorectal cancer cell migration ability through <scp>RAS</scp>/<scp>MEK</scp>/<scp>ERK</scp>" @default.
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• W4294132531 doi "https://doi.org/10.1111/1440-1681.13717" @default.
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