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Epigenetic silencing of Th1 chemokines shapes tumor immunity, immunotherapy and patient outcome [GSK126]

ABSTRACT: To define the gene profile altered by EZH2 and H3K27me3 in response to IFNg, we performed several microarrays in primary ovarian cancer cells transfected with shEZH2 or treated with GSK126. We found that 155 and 124 genes were altered by shEZH2 and GSK126 treatment, respectively, and 20 genes were increased or decreased by both shEZH2 and GSK126 treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE71869 | GEO | 2015/08/11

SECONDARY ACCESSION(S): PRJNA292384

REPOSITORIES: GEO

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Epigenetic silencing of Th1 chemokines shapes tumor immunity, immunotherapy and patient outcome [GSK126]

Project description:To define the gene profile altered by EZH2 and H3K27me3 in response to IFNg, we performed several microarrays in primary ovarian cancer cells transfected with shEZH2 or treated with GSK126. We found that 155 and 124 genes were altered by shEZH2 and GSK126 treatment, respectively, and 20 genes were increased or decreased by both shEZH2 and GSK126 treatment. Primary ovarian cancer cells were pretreated with GSK126, or transduced with a shEZH2 lentivirus, and stimulated with IFNg for 24 hours. RNA were isolated by Rneasy kit according to the manufacturer's protocol, and applied for affymetrix microarray at University of Michigan DNA Sequencing Core

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Epigenetic silencing of Th1 chemokines shapes tumor immunity, immunotherapy and patient outcome [shEZH2]

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Epigenetic silencing of Th1 chemokines shapes tumor immunity, immunotherapy and patient outcome

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Epigenetic silencing of Th1 chemokines shapes tumor immunity, immunotherapy and patient outcome

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Epigenetic silencing of TH1-type chemokines shapes tumour immunity and immunotherapy.

Project description:Epigenetic silencing including histone modifications and DNA methylation is an important tumorigenic mechanism. However, its role in cancer immunopathology and immunotherapy is poorly understood. Using human ovarian cancers as our model, here we show that enhancer of zeste homologue 2 (EZH2)-mediated histone H3 lysine 27 trimethylation (H3K27me3) and DNA methyltransferase 1 (DNMT1)-mediated DNA methylation repress the tumour production of T helper 1 (TH1)-type chemokines CXCL9 and CXCL10, and subsequently determine effector T-cell trafficking to the tumour microenvironment. Treatment with epigenetic modulators removes the repression and increases effector T-cell tumour infiltration, slows down tumour progression, and improves the therapeutic efficacy of programmed death-ligand 1 (PD-L1; also known as B7-H1) checkpoint blockade and adoptive T-cell transfusion in tumour-bearing mice. Moreover, tumour EZH2 and DNMT1 are negatively associated with tumour-infiltrating CD8(+) T cells and patient outcome. Thus, epigenetic silencing of TH1-type chemokines is a novel immune-evasion mechanism of tumours. Selective epigenetic reprogramming alters the T-cell landscape in cancer and may enhance the clinical efficacy of cancer therapy.

| S-EPMC4779053 | biostudies-literature

Expression analysis after co-treatment of GSK126 and pomalidomide

Project description:To determine combination effect of GSK126 and pomalidomide at the RNA levels in EZH2 Y641 mutant DLBCL, We performed gene expression profiling in WSU-DLCL2 cell line after co-treatment of GSK126 and pomalidomide

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Transcriptomic profiling of MGT#1-mVenus-reporter harboring A549 and H1944 cells upon stimulation with GSK126 and TGF-β1.

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