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• W2909413229 abstract "Pancreatic ductal adenocarcinoma (PDAC) is the second leading cause of cancer-related deaths worldwide. Despite immune checkpoints based immunotherapy highlights a new therapeutic strategy and achieves a remarkable therapeutic effect in various types of malignant tumors. Pancreatic cancer is one of the non-immunogenic cancers and is resistant to immunotherapy. Programmed death ligand 1 (PD-L1) is expressed on the surface of tumor cells and its level is a key determinant of the checkpoint immunotherapy efficacy. Here, we reported that the specific inhibitor of histone deacetylase 3 (HDAC3) decreased the protein and mRNA level of PD-L1 in pancreatic cancer cells. Furthermore, we showed that HDAC3 was critical for PD-L1 regulation and positively correlated with PD-L1 in PDAC patient specimens. Finally, we demonstrated that HDAC3/signal transducer and activator of transcription 3 (STAT3) pathway transcriptionally regulated PD-L1 expression. Collectively, our data contributes to a better understanding of the function of HDAC3 in cancer immunity and the regulatory mechanism of PD-L1. More importantly, these data suggest that the HDAC3 inhibitors might be used to improve immunotherapy in pancreatic cancer." @default.
• W2909413229 created "2019-01-25" @default.
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• W2909413229 date "2019-03-01" @default.
• W2909413229 modified "2023-09-22" @default.
• W2909413229 title "HDAC3 modulates cancer immunity via increasing PD-L1 expression in pancreatic cancer" @default.
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• W2909413229 doi "https://doi.org/10.1016/j.pan.2019.01.011" @default.
• W2909413229 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30670333" @default.
• W2909413229 hasPublicationYear "2019" @default.
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