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Non-canonical immune response to inhibition of DNA methylation via stabilization of dsRNAs from endogenous retroviruses

ABSTRACT: Non-canonical immune response to inhibition of DNA methylation via stabilization of dsRNAs from endogenous retroviruses

PROVIDER: PRJNA638824 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11996357_1.fastq.gz	Fastqsanger.gz
	SRR11996357_2.fastq.gz	Fastqsanger.gz
	SRR11996358_1.fastq.gz	Fastqsanger.gz
	SRR11996358_2.fastq.gz	Fastqsanger.gz
	SRR11996359_1.fastq.gz	Fastqsanger.gz

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Non-canonical immune response to inhibition of DNA methylation via stabilization of dsRNAs from endogenous retroviruses

Project description:5-Aza-2'-deoxycytidine, also known as decitabine, is a DNA hypomethylating agent (HMA) used to treat acute myeloid leukemia (AML) and pre-leukemic disorder myelodysplastic syndrome (MDS). Decitabine activates the transcription of endogenous retroviruses (ERV), which can induce immune response by acting as cellular double-stranded RNAs. Here, we employ an image-based screening system to identify dsRNA-binding factors that mediate the downstream effect of ERV induction. We find that STAUFEN1 (STAU1) knockdown decreases the interferon signature and rescues decitabine-mediated cell death. Our subsequent analyses reveal that STAU1 directly binds to ERV RNAs and stabilizes the RNAs together with a long noncoding RNA, TINCR. Analysis of a clinical patient cohort further supports that MDS and AML patients with low STAU1 and TINCR expressions exhibited poor response to the HMA therapy. Our study reveals that decitabine-mediated cell death is a consequence of complex interactions among different dsRNA binding proteins for access to their common dsRNA targets.

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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.

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TERT activates endogenous retroviruses contributing to immunosuppressive tumour microenvironment III

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