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Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [ChIP-Seq]

ABSTRACT: Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [ChIP-Seq]

PROVIDER: PRJNA563608 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10059514.fastq.gz	Fastqsanger.gz
	SRR10059515.fastq.gz	Fastqsanger.gz
	SRR10059516.fastq.gz	Fastqsanger.gz
	SRR10059517.fastq.gz	Fastqsanger.gz
	SRR10059518.fastq.gz	Fastqsanger.gz

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Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia

Project description:Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia

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Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [DNase-Seq]

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Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [RNA-Seq]

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Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [RNA-Seq]

Project description:Endogenous retroviruses (ERVs) and other transposons can act as tissue-specific regulators of gene expression in cis, with potential to affect biological processes. In cancer, epigenetic alterations and transcription factor misregulation may uncover the regulatory potential of typically repressed ERVs, which could contribute to tumour evolution and progression. Here, we asked whether transposons help to rewire oncogenic transcriptional circuits in acute myeloid leukaemia (AML). Using epigenomic data from both primary cells and cell lines, we have identified six ERV families that are frequently found in an open chromatin state in AML when compared to differentiated myeloid cells. A subset of these AML-associated ERVs harbour enhancer-specific histone modifications, and are bound by transcription factors that play key roles in haematopoiesis and in the pathogenesis of AML. Using CRISPR-mediated genetic and epigenetic editing, we have established causal links between ERV deregulation in AML and expression changes of adjacent genes. Finally, we show that deletion and epigenetic silencing of an ERV associated with the APOC1 gene leads to growth suppression by inducing apoptosis in leukemia cell lines. Our results suggest that ERV derepression provides an additional layer of gene regulation in AML that may be exploited by cancer cells to help drive oncogenic phenotypes.

2019-09-04 | GSE136763 | GEO

Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [DNase-Seq]

2019-09-04 | GSE136760 | GEO

Endogenous retroviruses are a source of oncogenic enhancers in acute myeloid leukemia [ChIP-Seq]

2019-09-04 | GSE136759 | GEO

Endogenous retroviruses mediate transcriptional rewiring in response to oncogenic signaling in colorectal cancer [CUT&RUN]

Project description:Cancer cells exhibit rewired transcriptional regulatory networks that promote tumor growth and survival. However, the processes that configure these pathological networks remain poorly understood. Through a pan-cancer epigenomic analysis, we found that primate-specific endogenous retroviruses (ERVs) are an abundant source of enhancers that mediate transcriptional dysregulation in cancer. In colorectal cancer and other epithelial tumors, AP1 signaling drives aberrant activation of enhancers derived from the primate-specific ERV family LTR10. CRISPR studies revealed that LTR10 elements control colorectal cancer-specific gene expression at multiple loci associated with tumorigenesis. Within the human population, individual LTR10 elements show extensive structural variation due to repeat instability of an internal variable number tandem repeat (VNTR) region that affects AP1 binding. Our findings reveal that ERV-derived enhancers link oncogenic signaling to transcriptional dysregulation and shape the evolution of cancer-specific regulatory networks.

2021-10-31 | GSE186608 | GEO

Endogenous retroviruses mediate transcriptional rewiring in response to oncogenic signaling in colorectal cancer [RNA-seq]

2021-10-31 | GSE186618 | GEO

Identification of human endogenous retroviruses working as enhancers in cancer cells

Project description:Human endogenous retroviruses (HERVs) are a sort of transposable elements. HERVs harbor abundant regulatory elements in their sequences and have a potential to work as enhancers modulating the expressions of the adjacent genes. Some HERV-enhancers are particularly activated in cancer cells and suspected to be associated with cancer progression. To verify the enhancer activity of HERVs on the gene expressions in lung adenocarcinoma cells, we established the HERV-excised A549 cell lines using a CRISPR-Cas9 system and performed RNA sequencing (RNA-Seq) analysis of these cells.

2020-09-29 | GSE141141 | GEO

Endogenous retroviruses act as enhancers to drive species-specific germline transcriptomes in mammals

Project description:Gene regulation in the germline ensures the production of high-quality gametes, long-term maintenance of the species, and speciation. Germline transcriptomes undergo dynamic changes after the mitosis-to-meiosis transition in males and have been subject to evolutionary divergence among mammals. However, the mechanism that underlies germline regulatory divergence remains undetermined. Here, we show that endogenous retroviruses influence species-specific germline transcriptomes in mammals. We show that the endogenous retroviruses function as active enhancers to drive evolutionarily young (mouse or rodent specific) spermatogenesis-specific genes after the mitosis-to-meiosis transition in male mice. These ERV loci bear binding motifs for critical regulators of spermatogenesis such as A-MYB. The genome-wide transposition of ERVs might have rewired germline gene expression in a species-specific manner. Notably, these features are present in human spermatogenesis, but independently evolved ERVs are associated with expression of germline genes, demonstrating the prevalence of ERV-driven mechanisms in mammals. Together, we propose a model whereby species-specific transcriptomes are fine-tuned by endogenous retroviruses in the mammalian germline.

2020-05-28 | GSE142173 | GEO

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