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DOI | 10.1038/s41467-019-11191-z |
STT3-dependent PD-L1 accumulation on cancer stem cells promotes immune evasion | |
Hsu, Jung-Mao1; Xia, Weiya1; Hsu, Yi-Hsin1; Chan, Li-Chuan1,2; Yu, Wen-Hsuan1,2; Cha, Jong-Ho1,3; Chen, Chun-Te1; Liao, Hsin-Wei1,2,4; Kuo, Chu-Wei5; Khoo, Kay-Hooi5; Hsu, Jennifer L.1,6,7; Li, Chia-Wei1; Lim, Seung-Oe1; Chang, Shih-Shin1,2; Chen, Yi-Chun1; Ren, Guo-Xin8; Hung, Mien-Chie1,2,6,7,9 | |
2019-07-19 | |
发表期刊 | NATURE COMMUNICATIONS
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ISSN | 2041-1723 |
出版年 | 2018 |
卷号 | 9 |
文章类型 | Article |
语种 | 英语 |
国家 | USA; South Korea; Taiwan; Peoples R China |
英文摘要 | 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/ss-catenin/STT3/PD-L1 signaling axis, in which EMT transcriptionally induces N-glycosyltransferase STT3 through beta-catenin, and subsequent STT3-dependent PD-L1 Nglycosylation 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/beta-catenin/STT3/PD-L1 axis through TOP2B degradation-dependent nuclear beta-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. |
领域 | 资源环境 |
收录类别 | SCI-E |
WOS记录号 | WOS:000432115300012 |
WOS关键词 | EPITHELIAL-MESENCHYMAL TRANSITION ; TOPOISOMERASE-II ; ANTITUMOR IMMUNITY ; INITIATING CELLS ; L1210 LEUKEMIA ; GASTRIC-CANCER ; UP-REGULATION ; HUMAN GENOME ; T-CELLS ; EXPRESSION |
WOS类目 | Multidisciplinary Sciences |
WOS研究方向 | Science & Technology - Other Topics |
URL | 查看原文 |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | http://119.78.100.173/C666/handle/2XK7JSWQ/204457 |
专题 | 资源环境科学 |
作者单位 | 1.Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, Houston, TX 77030 USA; 2.Univ Texas Houston, Grad Sch Biomed Sci, Houston, TX 77030 USA; 3.Seoul Natl Univ, Coll Pharm, Tumor Microenvironm Global Core Res Ctr, Seoul 151742, South Korea; 4.Harvard Med Sch, Ctr Syst Biol, Massachusetts Gen Hosp Res Inst, Boston, MA 02114 USA; 5.Acad Sin, Inst Biol Chem, Taipei 115, Taiwan; 6.China Med Univ, Grad Inst Biomed Sci, Taichung 404, Taiwan; 7.China Med Univ, Ctr Mol Med, Taichung 404, Taiwan; 8.Shanghai Jiao Tong Univ, Dept Oral & Maxillofacial Head & Neck Oncol, Affiliated Peoples Hosp 9, Shanghai 200011, Peoples R China; 9.Asia Univ, Dept Biotechnol, Taichung 413, Taiwan |
推荐引用方式 GB/T 7714 | Hsu, Jung-Mao,Xia, Weiya,Hsu, Yi-Hsin,et al. STT3-dependent PD-L1 accumulation on cancer stem cells promotes immune evasion[J]. NATURE COMMUNICATIONS,2019,9. |
APA | Hsu, Jung-Mao.,Xia, Weiya.,Hsu, Yi-Hsin.,Chan, Li-Chuan.,Yu, Wen-Hsuan.,...&Hung, Mien-Chie.(2019).STT3-dependent PD-L1 accumulation on cancer stem cells promotes immune evasion.NATURE COMMUNICATIONS,9. |
MLA | Hsu, Jung-Mao,et al."STT3-dependent PD-L1 accumulation on cancer stem cells promotes immune evasion".NATURE COMMUNICATIONS 9(2019). |
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