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The transcription factor Myb enhances CD8+ T cell stemness and antitumor immunity

ABSTRACT: The transcription factor Myb enhances CD8+ T cell stemness and antitumor immunity

PROVIDER: PRJNA439010 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6862690.fastq.gz	Fastqsanger.gz
	SRR6862690_1.fastq.gz	Fastqsanger.gz
	SRR6862690_2.fastq.gz	Fastqsanger.gz
	SRR6862691.fastq.gz	Fastqsanger.gz
	SRR6862691_1.fastq.gz	Fastqsanger.gz

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The transcription factor Myb enhances CD8+ T cell stemness and antitumor immunity

Project description:Stem cells are maintained by transcriptional programs promoting self-renewal and repressing differentiation. Here, we show that the transcription factor Myb is essential for generating and maintaining stem cells within the CD8+ T-cell memory compartment. We found that, following viral infection, CD8+ T cells lacking Myb underwent terminal differentiation and exhibited impaired capacity to form CD62L+ stem cell-like memory cells. Myb acted both as a transcriptional activator of Tcf7 to enhance the development of memory cells and as a repressor of effector differentiation through Zeb2 suppression. Myb mutants’ complementation revealed that the Myb transactivation domain was necessary to restrain terminal differentiation, whereas the negative regulatory domain was critical for cell survival. Conversely, Myb overexpression enhanced CD8+ T-cell memory formation, polyfunctionality, and recall responses promoting curative antitumor immunity. These findings identify Myb as a pivotal regulator of CD8+ T-cell stemness and highlight the therapeutic potential of increasing Myb activity in CD8+ T cells.

2018-11-01 | GSE112049 | GEO

Dnase1l3 enhances antitumor immunity and suppresses tumor progression

Project description:Dnase1l3 enhances antitumor immunity and suppresses tumor progression

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Dnase1l3 enhances antitumor immunity and suppresses tumor progression [scRNAseq]

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c-Myb upregulation stimulates antitumor immunity in a murine colorectal cancer model

Project description:c-Myb upregulation stimulates antitumor immunity in a murine colorectal cancer model

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

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c-Myb upregulation stimulates antitumor immunity in a murine colorectal cancer model

Project description:While the transcription factor c-Myb is overexpressed in different types of solid tumors, including colorectal cancer, its exact role in tumorigenesis is unclear. In this study, we show that tumor-intrinsic c-Myb expression in mouse models of colon cancer and melanoma suppresses tumor growth. While no difference in proliferation, apoptosis, and angiogenesis of tumors were evident, we observed changes in intratumoral immune cell infiltrates. MC38 tumors with upregulated c-Myb expression showed increased counts of CD103+ dendritic cells and eosinophils, but decreased tumor-associated macrophages (TAMs). Concomitantly, an increase in cytotoxic CD8+ T cells upon c-Myb upregulation was observed, which correlated with a pro-inflammatory tumor microenvironment and increased numbers of M1 polarized TAMs. Mechanistically, c-Myb upregulation in immunogenic MC38 colon cancer cells resulted in enhanced expression of immunomodulatory genes, including b2-microglobulin, interferon-β and decreased expression of the chemokine receptor CCR2. The observed increased counts of cytotoxic CD8+ T cells contributed to tumor growth attenuation. In poorly immunogenic CT26, LLC and B16-BL6 tumor cells, c-Myb upregulation did not affect immune responses. Interestingly, c-Myb upregulation has led to a reduced B16-BL6 tumor growth but it did not affect tumor growth of CT26 and LLC tumors. Altogether, we postulate that c-Myb functions as a tumor suppressor in a tumor cell-type specific manner and modulates anti-tumor immunity.

2023-07-28 | GSE232823 | GEO

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

Targeted epigenetic induction of mitochondrial biogenesis enhances antitumor immunity in mouse model

Project description:Targeted epigenetic induction of mitochondrial biogenesis enhances antitumor immunity in mouse model

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

2021-10-20 | GSE182197 | GEO

Increased antigenicity of NURF-depleted tumors enhances CD8 T cell-mediated antitumor immunity

Project description:Depleting the NURF chromatin remodeling complex results in enhanced antitumor immunity using mouse tumor models syngenic to two strain backgrounds. Selective depletion of immune cells from tumor-bearing mice discovers that both CD8+ and CD4+ cells are necessary for enhanced antitumor immunity to NURF-depleted cells. Our results suggest that NURF-depleted cells have significant differences in antigenicity compared to control cells.

2016-04-29 | GSE71864 | GEO

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