Loss of ZNF408 Is Linked to Immune Escape in Breast Carcinogenesis [ATAC-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1070342 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27777082_1.fastq.gz | Fastqsanger.gz | |||
| SRR27777082_2.fastq.gz | Fastqsanger.gz | |||
| SRR27777083_1.fastq.gz | Fastqsanger.gz | |||
| SRR27777083_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
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Project description:Loss of ZNF408 Is Linked to Immune Escape in Breast Carcinogenesis.
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Project description:Understanding cancer immune escape is important to the comprehension of cancer development and to the development of cancer immunotherapy. We report here that ZNF408, encoded by a gene linked to familial exudative vitreoretinopathy (FEVR) and autosomal recessive retinitis pigmentosa (RP), is physically associated with the chromatin remodeler SETD1A/COMPASS complex in breast cancer cells. The ZNF408/SETD1A/COMPASS complex orchestrates the transcriptional activation of a cohort of genes via histone H3K4 trimethylation, particularly STING1 that are critically involved in innate immune response, leading to the release of multiple cytokines and activation of cytotoxic lymphocyte cells in tumor microenvironment. ZNF408 enhances STING expression and promotes anti-tumor immune responses both in vitro and in vivo. Importantly, the expression of ZNF408 is downregulated in breast carcinomas, and its level of expression is positively correlated with that of STING1 and negatively correlated with the histological grade of breast cancer. High ZNF408 is also correlated with high CD8+ T cell infiltration and favorable prognosis of breast cancer patients. Our study uncovers an important role for ZNF408 in innate immune response, supporting further investigations of the ZNF408-SETD1A/COMPASS-STING1 axis in cancer immune escape as well as in other ZNF408-associated diseases including FEVR and RP.
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Project description:Understanding cancer immune escape is important to the comprehension of cancer development and to the development of cancer immunotherapy. We report here that ZNF408, encoded by a gene linked to familial exudative vitreoretinopathy (FEVR) and autosomal recessive retinitis pigmentosa (RP), is physically associated with the chromatin remodeler SETD1A/COMPASS complex in breast cancer cells. The ZNF408/SETD1A/COMPASS complex orchestrates the transcriptional activation of a cohort of genes via histone H3K4 trimethylation, particularly STING1 that are critically involved in innate immune response, leading to the release of multiple cytokines and activation of cytotoxic lymphocyte cells in tumor microenvironment. ZNF408 enhances STING expression and promotes anti-tumor immune responses both in vitro and in vivo. Importantly, the expression of ZNF408 is downregulated in breast carcinomas, and its level of expression is positively correlated with that of STING1 and negatively correlated with the histological grade of breast cancer. High ZNF408 is also correlated with high CD8+ T cell infiltration and favorable prognosis of breast cancer patients. Our study uncovers an important role for ZNF408 in innate immune response, supporting further investigations of the ZNF408-SETD1A/COMPASS-STING1 axis in cancer immune escape as well as in other ZNF408-associated diseases including FEVR and RP.
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Project description:Understanding cancer immune escape is important to the comprehension of cancer development and to the development of cancer immunotherapy. We report here that ZNF408, encoded by a gene linked to familial exudative vitreoretinopathy (FEVR) and autosomal recessive retinitis pigmentosa (RP), is physically associated with the chromatin remodeler SETD1A/COMPASS complex in breast cancer cells. The ZNF408/SETD1A/COMPASS complex orchestrates the transcriptional activation of a cohort of genes via histone H3K4 trimethylation, particularly STING1 that are critically involved in innate immune response, leading to the release of multiple cytokines and activation of cytotoxic lymphocyte cells in tumor microenvironment. ZNF408 enhances STING expression and promotes anti-tumor immune responses both in vitro and in vivo. Importantly, the expression of ZNF408 is downregulated in breast carcinomas, and its level of expression is positively correlated with that of STING1 and negatively correlated with the histological grade of breast cancer. High ZNF408 is also correlated with high CD8+ T cell infiltration and favorable prognosis of breast cancer patients. Our study uncovers an important role for ZNF408 in innate immune response, supporting further investigations of the ZNF408-SETD1A/COMPASS-STING1 axis in cancer immune escape as well as in other ZNF408-associated diseases including FEVR and RP.
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Project description:X chromosome inactivation (XCI) silences most genes on one X chromosome in female mammals, but some genes escape XCI. To identify escape gene in vivo and to explore molecular mechanisms that regulate this process we analyzed the allele-specific expression and chromatin structure of X-linked genes in mouse tissues and cells with skewed XCI and distinguishable alleles based on single nucleotide polymorphisms. Using a new method to estimate allelic expression, we demonstrate a continuum between complete silencing and significant expression from the inactive X (Xi). Few genes (2-3%) escape XCI to a significant level and only a minority differs between mouse tissues, suggesting stringent silencing and escape controls. Allelic profiles of DNase I hypersensitivity and RNA polymerase II occupancy of genes on the Xi correlate with escape from XCI. Allelic binding profiles of the DNA binding protein CCCTC-binding factor (CTCF) in different cell types indicate that CTCF binding at the promoter correlates with escape. Importantly, CTCF binding at the boundary between escape and silenced domains may prevent the spreading of active escape chromatin into silenced domains. Examination of CTCF and RNA PolIIS5p occupancy in mouse hybrid cells and adult tissues.
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