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Dnase1l3 enhances antitumor immunity and suppresses tumor progression [scRNAseq]

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

PROVIDER: PRJNA803189 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17873453_1.fastq.gz	Fastqsanger.gz
	SRR17873453_2.fastq.gz	Fastqsanger.gz
	SRR17873454_1.fastq.gz	Fastqsanger.gz
	SRR17873454_2.fastq.gz	Fastqsanger.gz
	SRR17873455_1.fastq.gz	Fastqsanger.gz

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Dnase1l3 enhances antitumor immunity and suppresses tumor progression

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

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Dnase1l3 enhances antitumor immunity and suppresses tumor progression [scRNAseq]

Project description:For the chronic inflammation-related colon cancer model (AOM/DSS-colon cancer model), 3-month-old Dnase1l3 WT and KO mice were injected with AOM (8 mg/kg, body weight). One week later, mice were challenged with 2.5% DSS water for 7 days followed by a 14-day recovery with regular drinking water for three cycles. Body weight, rectal bleeding and diarrhea were monitored during the entire experiment. Mice with more than 25% weight loss were removed during the experiment. For the AOM model, 2-month-old Dnase1l3 WT and KO mice were injected intraperitoneally with AOM (8 mg/kg, body weight). Colon tissues were isolated 9 hours, or five days after injection. All animal experiments were conducted in accordance with guidelines of NIEHS/NIH Animal Care and Use Committee.

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

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Dnase1l3 enhances antitumor immunity and suppresses tumor progression

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DNASE1L3 enhances antitumor immunity and suppresses tumor progression in colon cancer.

Project description:DNASE1L3, an enzyme highly expressed in DCs, is functionally important for regulating autoimmune responses to self-DNA and chromatin. Deficiency of DNASE1L3 leads to development of autoimmune diseases in both humans and mice. However, despite the well-established causal relationship between DNASE1L3 and immunity, little is known about the involvement of DNASE1L3 in regulation of antitumor immunity, the foundation of modern antitumor immunotherapy. In this study, we identify DNASE1L3 as a potentially new regulator of antitumor immunity and a tumor suppressor in colon cancer. In humans, DNASE1L3 is downregulated in tumor-infiltrating DCs, and this downregulation is associated with poor patient prognosis and reduced tumor immune cell infiltration in many cancer types. In mice, Dnase1l3 deficiency in the tumor microenvironment enhances tumor formation and growth in several colon cancer models. Notably, the increased tumor formation and growth in Dnase1l3-deficient mice are associated with impaired antitumor immunity, as evidenced by a substantial reduction of cytotoxic T cells and a unique subset of DCs. Consistently, Dnase1l3-deficient DCs directly modulate cytotoxic T cells in vitro. To our knowledge, our study unveils a previously unknown link between DNASE1L3 and antitumor immunity and further suggests that restoration of DNASE1L3 activity may represent a potential therapeutic approach for anticancer therapy.

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SETDB1-TRIM28 complex suppresses antitumor immunity

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BPTF Depletion Enhances NK Cell Mediated Antitumor Immunity

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B-cell-intrinsic DNase1L3 is essential for T-cell-independent type II response in mice

Project description:T-cell independent type II (TI-II) antigens, such as capsular polysaccharides, have multivalent epitope, which induce B cell activation, plasma cell differentiation and antibody production by strongly cross-linking B cell receptors. However, the mechanism of B cell activation by TI-II antigens remains unclear. In this study, we demonstrate that DNA endonuclease DNase1L3 (also termed DNase g) is required for the TI-II response. The production of antigen-specific antibodies was severely diminished in DNase1L3-deficient mice upon immunization with TI-II antigens, but not with TD antigens. Bone-marrow chimeric mice and B cell transfer experiments revealed that B-cell-intrinsic DNase1L3 was required for the TI-II response. DNase1L3-deficient B cells were defective in cell proliferation and plasma cell differentiation in the TI-II response in vivo as well as in vitro, which was not rescued by co-culture with DNase1L3-sufficient B cells in vitro, disproving an involvement of a secretory DNase1L3. In vitro stimulation with TI-II antigen transiently increased expression of DNase1L3 and its translocation into the nucleus. RNA-seq analysis of ex-vivo B cells having been responded to TI-II antigen in vivo revealed a marked reduction of Myc-target gene sets in DNase1L3-deficient B cells. Expression of IRF4, the gene of which is a target of Myc, was diminished in the ex-vivo DNase1L3-deficient B cells, in which forced expression of IRF4 restored the TI-II response in vivo. These data revealed an unexpected role of DNase1L3 in a missing link between B cell receptor signaling and B cell activation in the TI-II response, giving a valuable clue to molecularly dissect this response.

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