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TERT activates endogenous retroviruses to promote an immunosuppressive tumour microenvironment

ABSTRACT: TERT activates endogenous retroviruses to promote an immunosuppressive tumour microenvironment

PROVIDER: PRJNA717744 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14082836_1.fastq.gz	Fastqsanger.gz
	SRR14082836_2.fastq.gz	Fastqsanger.gz
	SRR14082837_1.fastq.gz	Fastqsanger.gz
	SRR14082837_2.fastq.gz	Fastqsanger.gz
	SRR14082838_1.fastq.gz	Fastqsanger.gz

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TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment I

Project description:TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment I

| PRJNA717750 | ENA

TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment III

Project description:TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment III

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TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment II

Project description:TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment II

| PRJNA717754 | ENA

TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment III

Project description:Telomerase plays a pivotal role in tumorigenesis by both telomere-dependent and telomere-independent activities, although the underlying mechanisms are not completely understood. Using single-sample gene set enrichment analysis (ssGSEA) across 9,264 tumour samples, we observed that expression of telomerase reverse transcriptase (TERT) is closely associated with immune-suppressive signatures. We demonstrated that TERT can activate a subclass of endogenous retroviruses (ERVs) to form double-stranded RNAs (dsRNAs), which were sensed by the RIG-1/MDA5-MAVS signalling pathway and triggered interferon signalling in cancer cells. Furthermore, we showed that TERT-induced ERVs/interferon signalling stimulated the expression of chemokines, including CXCL10, which induced suppressed T cell infiltration with increased percentage of CD4+ and FOXP3+ cells. These data reveal an unanticipated role for telomerase as a transcriptional activator of ERVs and provide strong evidence that TERT-mediated ERVs/interferon signalling contributes to immune suppression in tumours.

2022-02-22 | GSE169714 | GEO

TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment II

2022-02-22 | GSE169713 | GEO

TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment I

2022-02-22 | GSE169711 | GEO

TERT activates endogenous retroviruses to promote an immunosuppressive tumour microenvironment.

Project description:Telomerase plays a pivotal role in tumorigenesis by both telomere-dependent and telomere-independent activities, although the underlying mechanisms are not completely understood. Using single-sample gene set enrichment analysis (ssGSEA) across 9,264 tumour samples, we observe that expression of telomerase reverse transcriptase (TERT) is closely associated with immunosuppressive signatures. We demonstrate that TERT can activate a subclass of endogenous retroviruses (ERVs) independent of its telomerase activity to form double-stranded RNAs (dsRNAs), which are sensed by the RIG-1/MDA5-MAVS signalling pathway and trigger interferon signalling in cancer cells. Furthermore, we show that TERT-induced ERV/interferon signalling stimulates the expression of chemokines, including CXCL10, which induces the infiltration of suppressive T-cell populations with increased percentage of CD4+ and FOXP3+ cells. These data reveal an unanticipated role for telomerase as a transcriptional activator of ERVs and provide strong evidence that TERT-mediated ERV/interferon signalling contributes to immune suppression in tumours.

| S-EPMC8982579 | biostudies-literature

TERT activates endogenous retroviruses to promote an immunosuppressive tumour microenvironment

Project description:Telomerase plays a pivotal role in tumorigenesis by both telomere-dependent and telomere-independent activities, although the underlying mechanisms are not completely understood. Using single-sample gene set enrichment analysis (ssGSEA) across 9,264 tumour samples, we observe that expression of telomerase reverse transcriptase (TERT) is closely associated with immunosuppressive signatures. We demonstrate that TERT can activate a subclass of endogenous retroviruses (ERVs) independent of its telomerase activity to form double-stranded RNAs (dsRNAs), which are sensed by the RIG-1/MDA5-MAVS signalling pathway and trigger interferon signalling in cancer cells. Furthermore, we show that TERT-induced ERV/interferon signalling stimulates the expression of chemokines, including CXCL10, which induces the infiltration of suppressive T cell populations with increased percentage of CD4+ and FOXP3+ cells. These data reveal an unanticipated role for telomerase as a transcriptional activator of ERVs and provide strong evidence that TERT-mediated ERV/interferon signalling contributes to immune suppression in tumours.

| S-SCDT-EMBOR-2021-52984V1 | biostudies-other

TERT activates endogenous retroviruses to promote an immunosuppressive tumour microenvironment

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-02-22 | GSE169715 | GEO

Gene expression data after acute withdrawal of TERT in mouse skin

Project description:TERT is an essential protein component of telomerase, a ribonuclearprotein complex that protects chromosomal ends. Ectopic expression of TERT in mouse skin activates hair follicle stem cells and induces active growth phase of hair cycles, called anagen. This activity of TERT is independent of its reverse transcriptase function, indicating that this is a non-telomeric function of TERT. We performed time-course microarray analysis using conditional bi-transgenic mice (iK5-TERT) to understand the mechanism of this novel non-telomeric function of TERT. Keywords: Time course, 2 cohorts (control, experimental)

2007-12-13 | GSE9725 | GEO

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