Search results for "Telomeric Repeat Binding Protein 2"

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Cancer cells induce immune escape via glycocalyx changes controlled by the telomeric protein TRF2

2019

International audience; 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 …

MaleHSPG;immunosurveillance;MDSC;NK cells;TRF2Mice NudeBiologyGlycocalyxGeneral Biochemistry Genetics and Molecular BiologyMetastasisGlycocalyx03 medical and health sciencesMice0302 clinical medicineDownregulation and upregulationNeoplasmsmedicineAnimalsHumansTelomeric Repeat Binding Protein 2STAT3Molecular BiologyCells Cultured030304 developmental biology0303 health sciencesGeneral Immunology and MicrobiologyGeneral NeuroscienceMyeloid-Derived Suppressor CellsArticlesTelomeremedicine.disease3. Good healthImmunosurveillanceGene Expression Regulation NeoplasticMice Inbred C57BLTLR2HEK293 CellsTumor progressionCancer cellCancer researchbiology.proteinNIH 3T3 Cells[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleTumor Escape030217 neurology & neurosurgery
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“Mitotic Slippage” and Extranuclear DNA in Cancer Chemoresistance: A Focus on Telomeres

2020

Mitotic slippage (MS), the incomplete mitosis that results in a doubled genome in interphase, is a typical response of TP53-mutant tumors resistant to genotoxic therapy. These polyploidized cells display premature senescence and sort the damaged DNA into the cytoplasm. In this study, we explored MS in the MDA-MB-231 cell line treated with doxorubicin (DOX). We found selective release into the cytoplasm of telomere fragments enriched in telomerase reverse transcriptase (hTERT), telomere capping protein TRF2, and DNA double-strand breaks marked by γH2AX, in association with ubiquitin-binding protein SQSTM1/p62. This occurs along with the alternative lengthening of telomeres (ALT) and DNA repa…

PolyploidizationALTSQSTM1/p62lcsh:ChemistryNeoplasmsSequestosome-1 Proteincellular senescenceTelomeric Repeat Binding Protein 2mtTP53 cancerTelomeraseAmoeboid conversionlcsh:QH301-705.5Telomere ShorteningSpectroscopyAntibiotics AntineoplasticGeneral MedicineTelomereComputer Science ApplicationsCell biologyinverted meiosisExtranuclear DNA<i>mtTP53</i> cancerSpo11DNA repairTelomere CappingMitosisBudding of mitotic progenygenotoxic treatmentamoeboid conversionInverted meiosisBiologyCellular senescenceArticleCatalysisInorganic ChemistryMeiosisCell Line Tumorextranuclear DNAHumansTelomerase reverse transcriptasePhysical and Theoretical ChemistryMolecular BiologyMitosisCell ProliferationGenotoxic treatmentOrganic ChemistryRecombinational DNA RepairCell Cycle CheckpointsDNA<i>SQSTM1/p62</i>polyploidizationTelomerelcsh:Biology (General)lcsh:QD1-999DoxorubicinDrug Resistance Neoplasmbiology.proteinHomologous recombinationbudding of mitotic progenyDNA DamageInternational Journal of Molecular Sciences
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