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TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment I

ABSTRACT: TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment I

PROVIDER: PRJNA717750 | ENA |

REPOSITORIES: ENA

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TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment III

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

| PRJNA717753 | ENA

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 II

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 | GSE169713 | GEO

TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment I

2022-02-22 | GSE169711 | GEO

TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment III

2022-02-22 | GSE169714 | GEO

TERT activates endogenous retroviruses to promote an immunosuppressive tumour microenvironment

Project description:TERT activates endogenous retroviruses to promote an immunosuppressive tumour microenvironment

| PRJNA717744 | ENA

TERT activates endogenous retroviruses to promote an immunosuppressive tumour microenvironment

Project description: Not available

| 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

Telomerase subunit TERT regulates MYC stability independent of its role on telomeres (array)

Project description:Constitutively active MYC and reactivated telomerase often co-exist in cancers. While the reactivation of telomerase is thought to be essential for replicative immortality, MYC, in conjunction with co-factors, confers several growth advantages to cancer cells. However, it is unclear which co-factors sustain elevated MYC activity in tumors . Here, we identify TERT, the catalytic subunit of telomerase, as a novel regulator of MYC stability in cancers. Binding of TERT to MYC stabilizes its levels on chromatin, contributing to either activation or repression of its target genes. Mechanistically, TERT regulates MYC ubiquitination and stability, and this effect of TERT is independent of its role on telomeres. Genetic inhibition and knocking out of TERT phenocopied the loss of MYC, resulting in reduced disease burden of early- and late-stage MYC-driven murine lymphomas. Conversly, the ectopic expression of TERT could substitute for reduced MYC in these functions. Finally we show that TERT null mice, unlike Terc null mice, show delayed onset of MYC induced lymphomagenesis. Accordingly, inhibiting TERT function in primary human leukemia cells blocked the expression of MYC targets, while Terc depletion had no effects . Based on our data, we conclude that the re-expression of TERT, a direct MYC target in tumors, provides a feed-forward mechanism to potentiate MYC-dependent oncogenesis. P493 cells were stably infected with the following viruses: pLKO shControl and pLKO shTERT.

2015-04-23 | E-GEOD-60175 | biostudies-arrayexpress

Telomerase subunit TERT regulates MYC stability independent of its role on telomeres (ChIP-Seq)

Project description:Constitutively active MYC and reactivated telomerase often co-exist in cancers. While the reactivation of telomerase is thought to be essential for replicative immortality, MYC, in conjunction with co-factors, confers several growth advantages to cancer cells. However, it is unclear which co-factors sustain elevated MYC activity in tumours . Here, we identify TERT, the catalytic subunit of telomerase, as a novel regulator of MYC stability in cancers. Binding of TERT to MYC stabilizes its levels on chromatin, contributing to either activation or repression of its target genes. Mechanistically, TERT regulates MYC ubiquitination and stability, and this effect of TERT is independent of its role on telomeres. Genetic inhibition and knocking out of TERT phenocopied the loss of MYC, resulting in reduced disease burden of early- and late-stage MYC-driven murine lymphomas. Conversly, the ectopic expression of TERT could substitute for reduced MYC in these functions. Finally we show that TERT null mice, unlike Terc null mice, show delayed onset of MYC induced lymphomagenesis. Accordingly, inhibiting TERT function in primary human leukemia cells blocked the expression of MYC targets, while Terc depletion had no effects . Based on our data, we conclude that the re-expression of TERT, a direct MYC target in tumors, provides a feed-forward mechanism to potentiate MYC-dependent oncogenesis. ChIP was performed using anti-MYC (sc-764) in primary lymphoma cells from Eµ-Myc;Tert -/- mice, Eµ-Myc;Tert +/+ mice, or in P493 cells treated with shTert, P493 shTerc and shControl.

2015-04-23 | E-GEOD-60223 | biostudies-arrayexpress

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