Distinct contributions of DNA methylation and histone acetylation to the genomic occupancy of transcription factors

Cusack, Martin; King, Hamish W; Spingardi, Paolo; Kessler, Benedikt M.; Klose, Robert J.; Kriaucionis, Skirmantas

doi:10.1101/gr.257576.119

Cited by 51 publications

(47 citation statements)

References 88 publications

(117 reference statements)

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“…DNA methylation is an important epigenetic modification that maintains genome integrity and regulates gene expression ( 39 ). The genome-wide DNA methylation environment of glioma has shown extensive spatiotemporal heterogeneity.…”

Section: Discussionmentioning

confidence: 99%

“…Epigenetics mainly involves the modification of DNA or proteins and posttranslational modification of histone proteins, and its function in the occurrence, malignant progression, and prognosis of gliomas has been demonstrated (37,38). DNA methylation is an important epigenetic modification that maintains genome integrity and regulates gene expression (39). The genome-wide DNA methylation environment of glioma has shown extensive spatiotemporal heterogeneity.…”

Section: Discussionmentioning

confidence: 99%

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A Signature of Nine lncRNA Methylated Genes Predicts Survival in Patients With Glioma

et al. 2021

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Glioma is one of the most common malignant tumors of the central nervous system, and its prognosis is extremely poor. Aberrant methylation of lncRNA promoter region is significantly associated with the prognosis of glioma patients. In this study, we investigated the potential impact of methylation of lncRNA promoter region in glioma patients to establish a signature of nine lncRNA methylated genes for determining glioma patient prognosis. Methylation data and clinical follow-up data were obtained from The Cancer Genome Atlas (TCGA). The multistep screening strategy identified nine lncRNA methylated genes that were significantly associated with the overall survival (OS) of glioma patients. Subsequently, we constructed a risk signature that containing nine lncRNA methylated genes. The risk signature successfully divided the glioma patients into high-risk and low-risk groups. Compared with the low-risk group, the high-risk group had a worse prognosis, higher glioma grade, and older age. Furthermore, we identified two lncRNAs termed PCBP1-AS1 and LINC02875 that may be involved in the malignant progression of glioma cells by using the TCGA database. Loss-of-function assays confirmed that knockdown of PCBP1-AS1 and LINC02875 inhibited the proliferation, migration, and invasion of glioma cells. Therefore, the nine lncRNA methylated genes signature may provide a novel predictor and therapeutic target for glioma patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

A Signature of Nine lncRNA Methylated Genes Predicts Survival in Patients With Glioma

et al. 2021

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“…A YY1 binding site is embedded within the T and G monomers (DeBerardinis and Kazazian 1999). YY1 binding to mouse L1 promoter was recently shown to occur in mouse ESCs devoid of DNA methylation and upon inhibition of histone deacetylase (HDAC) activity using trichostatin A (Cusack et al 2020). In addition, cap analysis of gene expression (CAGE) sequencing data revealed a broad TSS in the mouse L1 promoters that contain a YY1-binding site (Zhou and Smith 2019).…”

Section: Long Interspersed Nuclear Elements (Lines)mentioning

confidence: 99%

TFs for TEs: the transcription factor repertoire of mammalian transposable elements

Hermant

Torres-Padilla

2021

Genes Dev.

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Transposable elements (TEs) are genetic elements capable of changing position within the genome. Although their mobilization can constitute a threat to genome integrity, nearly half of modern mammalian genomes are composed of remnants of TE insertions. The first critical step for a successful transposition cycle is the generation of a full-length transcript. TEs have evolved cis-regulatory elements enabling them to recruit host-encoded factors driving their own, selfish transcription. TEs are generally transcriptionally silenced in somatic cells, and the mechanisms underlying their repression have been extensively studied. However, during germline formation, preimplantation development, and tumorigenesis, specific TE families are highly expressed. Understanding the molecular players at stake in these contexts is of utmost importance to establish the mechanisms regulating TEs, as well as the importance of their transcription to the biology of the host. Here, we review the transcription factors known to be involved in the sequence-specific recognition and transcriptional activation of specific TE families or subfamilies. We discuss the diversity of TE regulatory elements within mammalian genomes and highlight the importance of TE mobilization in the dispersal of transcription factor-binding sites over the course of evolution.

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“…Recruitment of HDACs to methylated regions acts in concert with DNA methylation to repress transcription. This mechanism is also affected by HDACi treatment, resulting in either increased or decreased methylation, suggesting complex regulation patterns, which are still poorly understood [ 92 , 96 , 97 ].…”

Section: Manipulation Of Histone Modificationmentioning

confidence: 99%

Latency Reversing Agents: Kick and Kill of HTLV-1?

Schnell

Kohrt

Thoma-Kress

2021

IJMS

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Human T-cell leukemia virus type 1 (HTLV-1), the cause of adult T-cell leukemia/lymphoma (ATLL), is a retrovirus, which integrates into the host genome and persistently infects CD4+ T-cells. Virus propagation is stimulated by (1) clonal expansion of infected cells and (2) de novo infection. Viral gene expression is induced by the transactivator protein Tax, which recruits host factors like positive transcription elongation factor b (P-TEFb) to the viral promoter. Since HTLV-1 gene expression is repressed in vivo by viral, cellular, and epigenetic mechanisms in late phases of infection, HTLV-1 avoids an efficient CD8+ cytotoxic T-cell (CTL) response directed against the immunodominant viral Tax antigen. Hence, therapeutic strategies using latency reversing agents (LRAs) sought to transiently activate viral gene expression and antigen presentation of Tax to enhance CTL responses towards HTLV-1, and thus, to expose the latent HTLV-1 reservoir to immune destruction. Here, we review strategies that aimed at enhancing Tax expression and Tax-specific CTL responses to interfere with HTLV-1 latency. Further, we provide an overview of LRAs including (1) histone deacetylase inhibitors (HDACi) and (2) activators of P-TEFb, that have mainly been studied in context of human immunodeficiency virus (HIV), but which may also be powerful in the context of HTLV-1.

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Distinct contributions of DNA methylation and histone acetylation to the genomic occupancy of transcription factors

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Cited by 51 publications

References 88 publications

A Signature of Nine lncRNA Methylated Genes Predicts Survival in Patients With Glioma

A Signature of Nine lncRNA Methylated Genes Predicts Survival in Patients With Glioma

TFs for TEs: the transcription factor repertoire of mammalian transposable elements

Latency Reversing Agents: Kick and Kill of HTLV-1?

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