STT3-dependent PD-L1 accumulation on cancer stem cells promotes immune evasion
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...
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| Published in | Nature communications Vol. 9; no. 1; pp. 1908 - 17 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
15.05.2018
Nature Publishing Group Nature Portfolio |
| Subjects | |
| Online Access | Get full text |
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| 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.
PD-L1 accumulates on cancer stem cells and favours immune evasion but the mechanism underlying this accumulation are unknown. Here the authors show that epithelial-mesenchymal transition induces glycosylation and stabilisation of PD-L1; antagonising this process renders cancer cells sensitive to anti-Tim3-therapy. |
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| AbstractList | 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.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. 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. 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. PD-L1 accumulates on cancer stem cells and favours immune evasion but the mechanism underlying this accumulation are unknown. Here the authors show that epithelial-mesenchymal transition induces glycosylation and stabilisation of PD-L1; antagonising this process renders cancer cells sensitive to anti-Tim3-therapy. PD-L1 accumulates on cancer stem cells and favours immune evasion but the mechanism underlying this accumulation are unknown. Here the authors show that epithelial-mesenchymal transition induces glycosylation and stabilisation of PD-L1; antagonising this process renders cancer cells sensitive to anti-Tim3-therapy. |
| ArticleNumber | 1908 |
| Author | Lim, Seung-Oe Chen, Yi-Chun Khoo, Kay-Hooi Chang, Shih-Shin Hung, Mien-Chie Chan, Li-Chuan Yu, Wen-Hsuan Ren, Guo-xin Hsu, Yi-Hsin Hsu, Jung-Mao Liao, Hsin-Wei Hsu, Jennifer L. Kuo, Chu-Wei Li, Chia-Wei Xia, Weiya Chen, Chun-Te Cha, Jong-Ho |
| Author_xml | – sequence: 1 givenname: Jung-Mao surname: Hsu fullname: Hsu, Jung-Mao organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 2 givenname: Weiya surname: Xia fullname: Xia, Weiya organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 3 givenname: Yi-Hsin surname: Hsu fullname: Hsu, Yi-Hsin organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 4 givenname: Li-Chuan surname: Chan fullname: Chan, Li-Chuan organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, The University of Texas Graduate School of Biomedical Sciences at Houston – sequence: 5 givenname: Wen-Hsuan surname: Yu fullname: Yu, Wen-Hsuan organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, The University of Texas Graduate School of Biomedical Sciences at Houston – sequence: 6 givenname: Jong-Ho surname: Cha fullname: Cha, Jong-Ho organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Tumor Microenvironment Global Core Research Center, College of Pharmacy, Seoul National University – sequence: 7 givenname: Chun-Te surname: Chen fullname: Chen, Chun-Te organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 8 givenname: Hsin-Wei surname: Liao fullname: Liao, Hsin-Wei organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, The University of Texas Graduate School of Biomedical Sciences at Houston, Center for Systems Biology, Massachusetts General Hospital Research Institute, Harvard Medical School – sequence: 9 givenname: Chu-Wei surname: Kuo fullname: Kuo, Chu-Wei organization: Institute of Biological Chemistry, Academia Sinica – sequence: 10 givenname: Kay-Hooi surname: Khoo fullname: Khoo, Kay-Hooi organization: Institute of Biological Chemistry, Academia Sinica – sequence: 11 givenname: Jennifer L. surname: Hsu fullname: Hsu, Jennifer L. organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Graduate Institute of Biomedical Sciences and Center for Molecular Medicine, China Medical University – sequence: 12 givenname: Chia-Wei surname: Li fullname: Li, Chia-Wei organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 13 givenname: Seung-Oe surname: Lim fullname: Lim, Seung-Oe organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 14 givenname: Shih-Shin surname: Chang fullname: Chang, Shih-Shin organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, The University of Texas Graduate School of Biomedical Sciences at Houston – sequence: 15 givenname: Yi-Chun surname: Chen fullname: Chen, Yi-Chun organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center – sequence: 16 givenname: Guo-xin surname: Ren fullname: Ren, Guo-xin organization: Department of Oral and Maxillofacial, Head and Neck Oncology, Affiliated 9th People’s Hospital, School of Medicine, Shanghai Jiaotong University – sequence: 17 givenname: Mien-Chie surname: Hung fullname: Hung, Mien-Chie email: mhung@mdanderson.org organization: Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, The University of Texas Graduate School of Biomedical Sciences at Houston, Graduate Institute of Biomedical Sciences and Center for Molecular Medicine, China Medical University, Department of Biotechnology, Asia University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29765039$$D View this record in MEDLINE/PubMed |
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| Snippet | Enriched PD-L1 expression in cancer stem-like cells (CSCs) contributes to CSC immune evasion. However, the mechanisms underlying PD-L1 enrichment in CSCs... PD-L1 accumulates on cancer stem cells and favours immune evasion but the mechanism underlying this accumulation are unknown. Here the authors show that... |
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| SubjectTerms | 13/1 14/19 631/67 631/80/458/1524 82/29 96/106 96/35 Animals B7-H1 Antigen - genetics B7-H1 Antigen - immunology beta Catenin - genetics beta Catenin - immunology Cancer Cancer immunotherapy Cell Line, Tumor DNA Topoisomerases, Type II - genetics DNA Topoisomerases, Type II - immunology Enrichment Epithelial-Mesenchymal Transition Etoposide Female Gene Expression Regulation, Neoplastic Glycosylation Glycosyltransferase Hexosyltransferases - genetics Hexosyltransferases - immunology Humanities and Social Sciences Humans Immune Evasion Immunotherapy Membrane Proteins - genetics Membrane Proteins - immunology Mesenchyme Mice, Inbred BALB C Mice, Knockout multidisciplinary Neoplasms - genetics Neoplasms - immunology Neoplasms - physiopathology Neoplastic Stem Cells - cytology Neoplastic Stem Cells - immunology PD-L1 protein Poly-ADP-Ribose Binding Proteins - genetics Poly-ADP-Ribose Binding Proteins - immunology Science Science (multidisciplinary) Stem cells Transcription β-Catenin |
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| Title | STT3-dependent PD-L1 accumulation on cancer stem cells promotes immune evasion |
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