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

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

PROVIDER: PRJNA774787 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16578433_1.fastq.gz	Fastqsanger.gz
	SRR16578433_2.fastq.gz	Fastqsanger.gz
	SRR16578434_1.fastq.gz	Fastqsanger.gz
	SRR16578434_2.fastq.gz	Fastqsanger.gz
	SRR16578435_1.fastq.gz	Fastqsanger.gz

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Endogenous retroviruses mediate transcriptional rewiring in response to oncogenic signaling in colorectal cancer

Project description:Endogenous retroviruses mediate transcriptional rewiring in response to oncogenic signaling in colorectal cancer

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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]

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

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Endogenous retroviruses mediate IFN-independent protection against HSV-2 infection

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

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Regulation of human trophoblast gene expression by endogenous retroviruses [CUT&RUN]

Project description:Regulation of human trophoblast gene expression by endogenous retroviruses [CUT&RUN]

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Endogenous retroviruses mediate IFN-independent protection against HSV-2 infection

Project description:Endogenous retroviruses (ERVs) are genomic sequences that originated from retroviruses and are present in most eukaryotic genomes. Both beneficial and detrimental functions are attributed to ERVs, but whether ERVs contribute to antiviral immunity is not well studied. Here, we used herpes simplex virus type 2 (HSV-2) infection as a model and found that mice deficient in Toll-like receptor 7 (Tlr7-/-) that have high systemic levels of infectious ERVs are resistant to intravaginal HSV-2 infection, compared with wildtype C57BL/6 (B6) mice. We deleted the endogenous ecotropic murine leukemia virus (Emv2) locus on the Tlr7-/- background (Emv2-/-Tlr7-/-) and found that Emv2-/-Tlr7-/- mice lose protection against HSV-2 infection. Intravaginal application of purified ERVs prior to HSV-2 infection delays disease in both B6 and highly susceptible interferon-alpha receptor-deficient (Ifnar1-/-) mice. We did not observe enhanced type I interferon (IFN-I) signaling in the vaginal tissues from Tlr7-/- mice or B6 mice treated with purified ERVs, and instead found enrichment in genes associated with extracellular matrix organization. Together, our results revealed an IFN-independent modulation of the vaginal epithelium by ERVs that protects mice against vaginal HSV-2 infection and delays disease.

2021-10-06 | GSE185281 | GEO

Endogenous retroviruses mediate transcriptional rewiring in response to oncogenic signaling in colorectal cancer.

Project description:Cancer cells exhibit rewired transcriptional regulatory networks that promote tumor growth and survival. However, the mechanisms underlying the formation of these pathological networks remain poorly understood. Through a pan-cancer epigenomic analysis, we found that primate-specific endogenous retroviruses (ERVs) are a rich source of enhancers displaying cancer-specific activity. In colorectal cancer and other epithelial tumors, oncogenic MAPK/AP1 signaling drives the activation of enhancers derived from the primate-specific ERV family LTR10. Functional studies in colorectal cancer cells revealed that LTR10 elements regulate tumor-specific expression of multiple genes associated with tumorigenesis, such as ATG12 and XRCC4. Within the human population, individual LTR10 elements exhibit germline and somatic structural variation resulting from a highly mutable internal tandem repeat region, which affects AP1 binding activity. Our findings reveal that ERV-derived enhancers contribute to transcriptional dysregulation in response to oncogenic signaling and shape the evolution of cancer-specific regulatory networks.

| S-EPMC466953 | biostudies-literature

Hijacking of transcriptional condensates by endogenous retroviruses

Project description:Hijacking of transcriptional condensates by endogenous retroviruses

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H3.3 deposition at endogenous retroviruses in embryonic stem cells

Project description:We report DAXX-dependent deposition of histone H3.3 at at endogenous retroviruses in embryonic stem cells.

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