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SETDB1-TRIM28 complex suppresses antitumor immunity [RNA-seq]

ABSTRACT: SETDB1-TRIM28 complex suppresses antitumor immunity [RNA-seq]

PROVIDER: PRJNA754434 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15446577_1.fastq.gz	Fastqsanger.gz
	SRR15446577_2.fastq.gz	Fastqsanger.gz
	SRR15446578_1.fastq.gz	Fastqsanger.gz
	SRR15446578_2.fastq.gz	Fastqsanger.gz
	SRR15446579_1.fastq.gz	Fastqsanger.gz

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SETDB1-TRIM28 complex suppresses antitumor immunity

Project description:SETDB1-TRIM28 complex suppresses antitumor immunity

| PRJNA755287 | ENA

SETDB1-TRIM28 complex suppresses antitumor immunity [RNA-seq]

Project description:Epigenetic mechanism contributes to immune landscapes in cancer. Here we identify the SETDB1-TRIM28 complex as a critical suppressor of antitumor immunity. An epigenetic CRISPR-Cas9 screen of 1,218 chromatin regulators identified TRIM28 as a novel suppressor of PD-L1 expression. We revealed that expression of the SETDB1-TRIM28 complex negatively correlates with infiltration of effector CD8+ T cells. Inhibition of SETDB1-TRIM28 simultaneously upregulates PD-L1 and activates the cGAS-STING innate immune response to increase infiltration of CD8+ T cells. Mechanistically, SETDB1-TRIM28 inhibition leads to micronuclei formation in cytoplasm, a known activator of the cGAS-STING pathway. Thus, SETDB1-TRIM28 inhibition bridges the innate and adaptive immunity. Indeed, SETDB1 knockout enhances the antitumor effects of immune checkpoint blockade anti-PD-L1 in an ovarian cancer mouse model in a cGAS dependent manner. Our findings establish SETDB1-TRIM28 complex as a regulator of antitumor immunity and its loss activates cGAS-STING innate immunity to boost antitumor effects of immune checkpoint blockades.

2021-10-20 | GSE182089 | GEO

SETDB1-TRIM28 complex suppresses antitumor immunity [CRISPR/Cas9 screen]

2021-10-20 | GSE182197 | GEO

SETDB1-TRIM28 complex suppresses antitumor immunity [CRISPR/Cas9 screen]

Project description:SETDB1-TRIM28 complex suppresses antitumor immunity [CRISPR/Cas9 screen]

| PRJNA755293 | ENA

SETDB1-TRIM28 complex suppresses antitumor immunity

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

2021-10-20 | GSE182198 | GEO

Dnase1l3 enhances antitumor immunity and suppresses tumor progression

Project description:Dnase1l3 enhances antitumor immunity and suppresses tumor progression

| PRJNA803220 | ENA

Dnase1l3 enhances antitumor immunity and suppresses tumor progression [scRNAseq]

Project description:Dnase1l3 enhances antitumor immunity and suppresses tumor progression [scRNAseq]

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Dnase1l3 enhances antitumor immunity and suppresses tumor progression [bulk RNAseq]

Project description:Dnase1l3 enhances antitumor immunity and suppresses tumor progression [bulk RNAseq]

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LARP7 suppresses endothelial-to-mesenchymal transition by coupling with TRIM28

Project description:LARP7 plays a pivotal role in regulating endothelial-to-mesenchymal transition(EndMT) and EndMT-associated heart valve formation. LARP7 directly interactes with TRIM28 and cooperatively represses SLUG transcription, which thereby suppresses EndMT of endothelial cells. More importantly, inducible knockout of LARP7 or TRIM28 in the endocardium promotes EndMT in vivo and leads to the valvular hyperplasia.

2023-09-22 | GSE165400 | GEO

Epigenetic Silencing by SETDB1 Suppresses Tumor-cell Intrinsic Immunogenicity

Project description:Griffin GK, Wu J, Iracheta-Vellve A, Patti JC, Hsu J, Davis T, Dele-Oni D, Du PP, Halawi A, Ishizuka JJ, Kim S, Klaeger S, Knudsen NH, Miller BC, Nguyen T, Olander K, Papanastasiou M, Rachimi S, Robitschek EJ, Schneider EM, Yeary M, Zimmer M, Jaffe JD, Carr SA, Doench JG, Haining WN, Yates KB, Manguso RT, Bernstein BE. 2020. Epigenetic dysregulation is a defining feature of tumorigenesis and has been implicated in immune escape, yet mechanisms that drive immune evasion are poorly understood. To systematically identify epigenetic factors that modulate the immune sensitivity of tumor cells, we performed in vivo CRISPR-Cas9 screens targeting 936 chromatin regulators in mouse tumor models treated with immune checkpoint blockade. We identified the H3K9-methyltransferase SETDB1 and other members of the HUSH and KAP1 complexes as cell-intrinsic mediators of immune escape in tumor cells. We also found that amplification of SETDB1 (1q21) in human tumors is associated with reduced cytotoxic T-cell infiltration and resistance to immune checkpoint blockade. Mechanistically, we demonstrate that SETDB1 represses broad domains, hundreds of kilobases in size, many of which reside within the open genome compartment. These SETDB1 domains are enriched for transposable elements (TEs) and immune gene clusters associated with segmental duplication events, a central mechanism of mammalian genome evolution. SETDB1 loss derepresses latent TE-encoded regulatory elements and proximal immune genes within these repetitive regions, including canonical co-stimulatory ligands, and induces hundreds of putative TE-encoded viral antigens. Our study establishes SETDB1 as an epigenetic checkpoint that suppresses intrinsic immunogenicity in cancer cells, and thus represents a candidate target for immunotherapy.

2020-12-11 | MSV000086580 | MassIVE

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