Show simple item record Cherfils-Vicini, Julien Iltis, Charlene Cervera, Ludovic Pisano, Sabrina Croce, Olivier Sadouni, Nori Győrffy, Balázs Collet, Romy Renault, Valérie M Rey-Millet, Martin Leonetti, Carlo Zizza, Pasquale Allain, Fabrice Ghiringhelli, Francois Soubeiran, Nicolas Shkreli, Marina Vivier, Eric Biroccio, Annamaria Gilson, Eric 2020-04-15T11:49:57Z 2020-04-15T11:49:57Z 2019
dc.identifier 85064630802
dc.identifier.citation journalVolume=38;journalIssueNumber=11;pagination=e100012, pages: 20;journalTitle=EMBO JOURNAL;journalAbbreviatedTitle=EMBO J;
dc.identifier.uri doi:10.15252/embj.2018100012
dc.description.abstract Myeloid-derived suppressor cells (MDSCs) are immature myeloid cells with strong immunosuppressive activity that promote tumor growth. In this study, we describe a mechanism by which cancer cells control MDSCs in human cancers by upregulating TRF2, a protein required for telomere stability. Specifically, we showed that the TRF2 upregulation in cancer cells has extratelomeric roles in activating the expression of a network of genes involved in the biosynthesis of heparan sulfate proteoglycan, leading to profound changes in glycocalyx length and stiffness, as revealed by atomic force microscopy. This TRF2-dependent regulation facilitated the recruitment of MDSCs, their activation via the TLR2/MyD88/IL-6/STAT3 pathway leading to the inhibition of natural killer recruitment and cytotoxicity, and ultimately tumor progression and metastasis. The clinical relevance of these findings is supported by our analysis of cancer cohorts, which showed a correlation between high TRF2 expression and MDSC infiltration, which was inversely correlated with overall patient survival.
dc.title Cancer cells induce immune escape via glycocalyx changes controlled by the telomeric protein TRF2
dc.type Journal Article 2019-11-26T14:54:53Z
dc.language.rfc3066 en
dc.rights.holder NULL
dc.identifier.mtmt 30650205
dc.identifier.wos 000470014200009
dc.identifier.pubmed 31000523
dc.contributor.department SE/AOK/K/II. Sz. Gyermekgyógyászati Klinika
dc.contributor.institution Semmelweis Egyetem

Files in this item

This file is available only from Semmelweis network


This item appears in the following Collection(s)

Show simple item record

Search DSpace

Advanced Search


My Account