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• W4386019874 abstract "PD-L1 is an immune checkpoint inhibitor, whose surface expression may be exploited by cancer cells to escape T cell-mediated immune recognition. PD-L1 expression and nuclear localization can be affected by epigenetic modifications, such as acetylation. In this study, we showed that VPA, a class I/IIa HDAC inhibitor, upregulated PD-L1 expression on the surface of pancreatic cancer cells. To this effect contributed the increased transcription, in correlation with histone acetylation of the PD-L1 gene and the acetylation of PD-L1 protein, which led to an increased interaction with TRAPPC4, molecule involved in PD-L1 recycling to the cell membrane. Interestingly, the BRD4 inhibitor JQ-1, counteracted PD-L1 transcription and reduced its surface expression, suggesting that such a combination could improve the outcome of VPA treatment, also because it increased the cytotoxic effect of VPA. Also considering that this HDACi did not upregulate PD-L2 and that the supernatant of VPA-treated cancer cells did not increase PD-L1 expression on the surface of macrophages exposed to it." @default.
• W4386019874 created "2023-08-22" @default.
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• W4386019874 date "2023-08-21" @default.
• W4386019874 modified "2023-09-25" @default.
• W4386019874 title "Acetylation increases expression, interaction with TRAPPC4 and surface localization of PD-L1" @default.
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• W4386019874 doi "https://doi.org/10.1007/s12672-023-00766-4" @default.
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• W4386019874 hasPublicationYear "2023" @default.
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