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Glioblastoma cells acquire myeloid-affiliated transcriptional programs via epigenetic immunoediting to elicit immune evasion [WGS]

ABSTRACT: Glioblastoma cells acquire myeloid-affiliated transcriptional programs via epigenetic immunoediting to elicit immune evasion [WGS]

PROVIDER: PRJNA694309 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13515301_1.fastq.gz	Fastqsanger.gz
	SRR13515301_2.fastq.gz	Fastqsanger.gz
	SRR13515302_1.fastq.gz	Fastqsanger.gz
	SRR13515302_2.fastq.gz	Fastqsanger.gz
	SRR13515303_1.fastq.gz	Fastqsanger.gz

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Glioblastoma cells acquire myeloid-affiliated transcriptional programs via epigenetic immunoediting to elicit immune evasion

Project description:Glioblastoma cells acquire myeloid-affiliated transcriptional programs via epigenetic immunoediting to elicit immune evasion

| PRJNA694308 | ENA

Glioblastoma cells acquire myeloid-affiliated transcriptional programs via epigenetic immunoediting to elicit immune evasion [WGS]

Project description:Glioblastoma multiforme (GBM) is an aggressive brain tumour. Current immunotherapy approaches have been unsuccessful, highlighting the need to determine underlying mechanisms of immune evasion. Here, we developed syngeneic immunocompetent mouse models of GBM to explore this. GBM stem cells (GSCs) were serially transplanted through immunocompetent hosts, which uncovered an acquired capability to escape immune clearance through an enhanced immunosuppressive tumour microenvironment. Mechanistically, this was not elicited via genetic selection of tumour subclones, but through an epigenetic immunoediting process wherein stable transcriptional and epigenetic changes in GSCs are enforced following immune attack. These include activation of interferon signalling modules, myeloid-affiliated transcription factors and chemokines, which leads to increased recruitment of tumour-associated macrophages. Furthermore, we identify similar epigenetic and transcriptional signatures in human mesenchymal subtype GSCs. We conclude that epigenetic immunoediting may drive an acquired immune evasion program in the most aggressive mesenchymal GBM subtype by reshaping the tumour immune microenvironment.

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Glioblastoma cells acquire myeloid-affiliated transcriptional programs via epigenetic immunoediting to elicit immune evasion [RNA-seq]

Project description:Glioblastoma cells acquire myeloid-affiliated transcriptional programs via epigenetic immunoediting to elicit immune evasion [RNA-seq]

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Glioblastoma cells acquire myeloid-affiliated transcriptional programs via epigenetic immunoediting to elicit immune evasion [BiSulfite-seq]

Project description:Glioblastoma cells acquire myeloid-affiliated transcriptional programs via epigenetic immunoediting to elicit immune evasion [BiSulfite-seq]

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Glioblastoma cells acquire myeloid-affiliated transcriptional programs via epigenetic immunoediting to elicit immune evasion [BiSulfite-seq]

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Glioblastomas acquire myeloid-affiliated transcriptional programs via epigenetic immunoediting to elicit immune evasion.

Project description:Glioblastoma multiforme (GBM) is an aggressive brain tumor for which current immunotherapy approaches have been unsuccessful. Here, we explore the mechanisms underlying immune evasion in GBM. By serially transplanting GBM stem cells (GSCs) into immunocompetent hosts, we uncover an acquired capability of GSCs to escape immune clearance by establishing an enhanced immunosuppressive tumor microenvironment. Mechanistically, this is not elicited via genetic selection of tumor subclones, but through an epigenetic immunoediting process wherein stable transcriptional and epigenetic changes in GSCs are enforced following immune attack. These changes launch a myeloid-affiliated transcriptional program, which leads to increased recruitment of tumor-associated macrophages. Furthermore, we identify similar epigenetic and transcriptional signatures in human mesenchymal subtype GSCs. We conclude that epigenetic immunoediting may drive an acquired immune evasion program in the most aggressive mesenchymal GBM subtype by reshaping the tumor immune microenvironment.

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Immunoediting instructs tumor metabolic reprogramming to support immune evasion [ExomeSeq]

Project description:Immunoediting sculpts immunogenicity and thwarts host anti-tumor responses in tumor cells during tumorigenesis; however, it remains unknown whether metabolic programming of tumor cells can be guided by immunosurveillance. Here, we report that T cell-mediated immunosurveillance in early staged tumorigenesis instructs c-Myc upregulation and metabolic reprogramming in tumor cells. This previously unexplored tumor-immune interaction is controlled by a non-canonical IFNg-STAT3 signaling and supports tumor immune evasion. Our findings uncover that immunoediting instructs deregulated bioenergetic programs in tumor cells for empowering them to disarm the T cell-mediated immunosurveillance by imposing metabolic tug-of-war between tumor and infiltrating T cells and forming the suppressive tumor microenvironment.

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Immunoediting instructs tumor metabolic reprogramming to support immune evasion [smartseq]

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Immunoediting instructs tumor metabolic reprogramming to support immune evasion [ATAC-seq]

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