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Genome-wide identification of differentially methylated promoters and enhancers associated with response to anti-PD-1 therapy in non-small cell lung cancer

ABSTRACT: Genome-wide identification of differentially methylated promoters and enhancers associated with response to anti-PD-1 therapy in non-small cell lung cancer

PROVIDER: PRJNA520851 | ENA |

REPOSITORIES: ENA

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Genome-wide identification of differentially methylated promoters and enhancers associated with response to anti-PD-1 therapy in non-small cell lung cancer

Project description:Genome-wide identification of differentially methylated promoters and enhancers associated with response to anti-PD-1 therapy in non-small cell lung cancer

| PRJNA520852 | ENA

Genome-wide identification of differentially methylated promoters and enhancers associated with response to anti-PD-1 therapy in non-small cell lung cancer

Project description:Genome-wide identification of differentially methylated promoters and enhancers associated with response to anti-PD-1 therapy in non-small cell lung cancer

| PRJNA520848 | ENA

Genome-wide identification of differentially methylated promoters and enhancers associated with response to anti-PD-1 therapy in non-small cell lung cancer.

Project description:Although approved programmed cell death protein (PD)-1 inhibitors show durable responses, clinical benefits to these agents are only seen in one-third of patients in most cancer types. Therefore, strategies for improving the response to PD-1 inhibitor for treating various cancers including non-small cell lung cancer (NSCLC) are urgently needed. Compared with genome and transcriptome, tumor DNA methylome in anti-PD-1 response was relatively unexplored. We compared the pre-treatment methylation status of cis-regulatory elements between responders and non-responders to treatment with nivolumab or pembrolizumab using the Infinium Methylation EPIC Array, which can profile ~850,000 CpG sites, including ~350,000 CpG sites located in enhancer regions. Then, we analyzed differentially methylated regions overlapping promoters (pDMRs) or enhancers (eDMRs) between responders and non-responders to PD-1 inhibitors. We identified 1007 pDMRs and 607 eDMRs associated with the anti-PD-1 response. We also identified 1109 and 1173 target genes putatively regulated by these pDMRs and eDMRs, respectively. We found that eDMRs contribute to the epigenetic regulation of the anti-PD-1 response more than pDMRs. Hypomethylated pDMRs of Cytohesin 1 Interacting Protein (CYTIP) and TNF superfamily member 8 (TNFSF8) were more predictive than programmed cell death protein ligand 1 (PD-L1) expression for anti-PD-1 response and progression-free survival (PFS) and overall survival (OS) in a validation cohort, suggesting their potential as predictive biomarkers for anti-PD-1 immunotherapy. The catalog of promoters and enhancers differentially methylated between responders and non-responders to PD-1 inhibitors presented herein will guide the development of biomarkers and therapeutic strategies for improving anti-PD-1 immunotherapy in NSCLC.

| S-EPMC8080767 | biostudies-literature

Genome-wide identification of differentially methylated promoters and enhancers associated with response to anti-PD-1 therapy in non-small cell lung cancer

Project description:The purpose of this study is to compare transcriptional profiles of non-small-cell lung cancer between responder patients and non-responder patients during anti-PD-1 treatment.

2020-09-04 | GSE126043 | GEO

Genome-wide identification of differentially methylated promoters and enhancers associated with response to anti-PD-1 therapy in non-small cell lung cancer

2020-02-03 | GSE126044 | GEO

Repurposing of promoters and enhancers during mammalian evolution

Project description:Repurposing of promoters and enhancers during mammalian evolution

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Validation of differentially methylated DNA regions in colorectal precancerous lesions.

Project description:Validation of differentially methylated DNA regions in colorectal precancerous lesions.

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Differentially methylated genes in saliva are linked to childhood stress

Project description:Differentially methylated genes in saliva are linked to childhood stress

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Chromatin-bound RB targets promoters, enhancers, and CTCF-bound loci.

Project description:RB’s interaction with chromatin is key to understanding its molecular functions. Using a novel ChIP-sequencing protocol, we identify the precise chromatin loci bound by various forms of human RB. RB targets three fundamentally different types of loci (promoters, enhancers, CTCF-sites), that are largely distinguishable by the mutually exclusive presence of E2F1, c-JUN and CTCF. E2F/DP facilitates RB association with promoters, whereas AP-1 recruits RB to enhancers. RB’s association with promoters and enhancers fluctuates: G1-arrest enriched RB at promoters, while S-phase progression redistributed RB towards enhancers. RB binding to RB/CTCF sites was unaltered by cell cycle progression. RB-bound promoters include the classic E2F targets and are similar between cell types. However, RB-bound enhancers are associated with different gene categories, including, notably, MAPK signaling, and they vary between cell types. We propose that RB has a well-preserved role controlling E2F in G1, and cell type-specific effects at enhancers when cells enter S-phase.

2022-08-01 | GSE176035 | GEO

Protein O-GlcNAcylation Silences Methylated Promoters in Mammalian Genomes

Project description:Methylated mammalian promoters are transcriptionally silenced even in the presence of all the factors required for their expression. Repression requires the assembly of a methylation-dependent silencing complex that contains the TRIM28 (also known as KAP1 and TIF1β) protein. An internally controlled interaction screen identified O-linked β-N-acetylglucosamine transferase (O-GlcNAc transferase or OGT) as a protein that was complexed with TRIM28 in wild type em-bryonic stem cells but not in Dnmt1-/- cells that had severely demethylated genomes. In the ab-sence of DNA methylation, multiple proteins associated with TRIM28 failed to undergo modifica-tion by N-Acetylglucosamine (GlcNAc). Mass spectrometry identified several of these proteins as known mediators of transcriptional silencing. The most active transposon in the mouse ge-nome is the IAP LTR retrotransposon, which have been previously shown to be repressed by DNA methylation. A Bacteroides O-GlcNAc hydrolase was fused to a catalytically inactive Cas9 and targeted to methylated IAP retrotransposon promoter sequences via IAP-specific guide RNAs; fulminating reactivation of IAP transcription was induced. These data revealed that Glc-NAcylation is directly involved in the transcriptional repression of methylated promoters.

2020-05-29 | GSE93539 | GEO

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