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- W2804930677 abstract "Enriched PD-L1 expression in cancer stem-like cells (CSCs) contributes to CSC immune evasion. However, the mechanisms underlying PD-L1 enrichment in CSCs remain unclear. Here, we demonstrate that epithelial-mesenchymal transition (EMT) enriches PD-L1 in CSCs by the EMT/β-catenin/STT3/PD-L1 signaling axis, in which EMT transcriptionally induces N-glycosyltransferase STT3 through β-catenin, and subsequent STT3-dependent PD-L1 N-glycosylation stabilizes and upregulates PD-L1. The axis is also utilized by the general cancer cell population, but it has much more profound effect on CSCs as EMT induces more STT3 in CSCs than in non-CSCs. We further identify a non-canonical mesenchymal-epithelial transition (MET) activity of etoposide, which suppresses the EMT/β-catenin/STT3/PD-L1 axis through TOP2B degradation-dependent nuclear β-catenin reduction, leading to PD-L1 downregulation of CSCs and non-CSCs and sensitization of cancer cells to anti-Tim-3 therapy. Together, our results link MET to PD-L1 stabilization through glycosylation regulation and reveal it as a potential strategy to enhance cancer immunotherapy efficacy." @default.
- W2804930677 created "2018-06-01" @default.
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- W2804930677 date "2018-05-15" @default.
- W2804930677 modified "2023-10-16" @default.
- W2804930677 title "STT3-dependent PD-L1 accumulation on cancer stem cells promotes immune evasion" @default.
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- W2804930677 doi "https://doi.org/10.1038/s41467-018-04313-6" @default.
- W2804930677 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5954021" @default.
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- W2804930677 hasPublicationYear "2018" @default.
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