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Oncogenic enhancers prime quiescent metastatic cells to escape NK immune surveillance by eliciting a transcriptional memory [ATAC-seq]

ABSTRACT: With this experiment, we aimed to decipher the changes in chromatin accessibility during tumour progression in a model of basal-like breast cancer, based on immortalized mammary epithelial cells (IMEC). The tumorigenic IMEC, xenograft-derived and metastasis-derived cells were used for the analysis

ORGANISM(S): Homo sapiens

PROVIDER: GSE211605 | GEO | 2024/02/02

REPOSITORIES: GEO

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Oncogenic enhancers prime quiescent metastatic cells to escape NK immune surveillance by eliciting a transcriptional memory [Cut&Run]

Project description:With this experiment, we aimed to decipher the epigenetic changes occuring during tumour progression in a model of basal-like breast cancer, based on immortalized mammary epithelial cells (IMEC). The tumorigenic IMEC, xenograft-derived and metastasis-derived cells were used for the analysis

2024-02-02 | GSE211606 | GEO

Oncogenic enhancers prime quiescent metastatic cells to escape NK immune surveillance by eliciting a transcriptional memory [HiChIP]

Project description:With this experiment, we aimed to decipher the changes in 3D chromatin interactions between active regulatroy elements (enhancer, promoter) during tumour progression by performing H3K27ac HiChIP in a model of basal-like breast cancer, based on immortalized mammary epithelial cells (IMEC). The tumorigenic IMEC, xenograft-derived and metastasis-derived cells were used for the analysis.

2024-02-02 | GSE211607 | GEO

Oncogenic enhancers prime quiescent metastatic cells to escape NK immune surveillance by eliciting a transcriptional memory [total RNA-seq]

Project description:With this experiment, we aimed to decipher the changes in gene expression during tumour progression in a model of basal-like breast cancer, based on immortalized mammary epithelial cells (IMEC). The tumorigenic IMEC, xenograft-derived and metastasis-derived cells were used for the total RNA-seq analysis.

2024-02-02 | GSE211608 | GEO

Oncogenic enhancers prime quiescent metastatic cells to escape NK immune surveillance by eliciting a transcriptional memory

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

2024-02-02 | GSE211610 | GEO

Oncogenic enhancers prime quiescent metastatic cells to escape NK immune surveillance by eliciting a transcriptional memory [nascent RNA-seq]

Project description:We aimed to investigate the transcriptional memory of metastatic basal-like breast cancer cells by performing nascent RNA-seq by treating with all-trans Retinoic acid (pulse, priming, priming + pulse)

2024-02-02 | GSE211609 | GEO

Quiescent Tissue Stem Cells Evade Immune Surveillance.

Project description:Stem cells are critical for the maintenance of many tissues, but whether their integrity is maintained in the face of immunity is unclear. Here we found that cycling epithelial stem cells, including Lgr5+ intestinal stem cells, as well as ovary and mammary stem cells, were eliminated by activated T cells, but quiescent stem cells in the hair follicle and muscle were resistant to T cell killing. Immune evasion was an intrinsic property of the quiescent stem cells resulting from systemic downregulation of the antigen presentation machinery, including MHC class I and TAP proteins, and is mediated by the transactivator NLRC5. This process was reversed upon stem cell entry into the cell cycle. These studies identify a link between stem cell quiescence, antigen presentation, and immune evasion. As cancer-initiating cells can derive from stem cells, these findings may help explain how the earliest cancer cells evade immune surveillance.

| S-EPMC5824652 | biostudies-literature

MYC favors the onset of tumorigenesis by inducing epigenetic reprogramming of mammary epithelial cells towards a stem cell-like state [ChIP-seq]

2018-01-30 | GSE86412 | GEO

Quiescent tissue stem cells evade immune surveillance

Project description:Stem cells are critical for the maintenance of many tissues, and thus their integrity is crucial, but whether this integrity is maintained in the face of an immune response is not well defined. Here we set out to determine the outcome of T cell interactions with adult stem cells in their physiological niche. We find that fast cycling epithelial stem cells, including Lgr5+ intestinal stem cells, as well as ovary and mammary stem cells, are eliminated by activated T-cells, but slow cycling stem cells, specifically hair follicle and muscle stem cells, are resistant to T-cell killing. This is an intrinsic property of the quiescent stem cells resulting from systemic downregulation of the antigen presentation machinery, including MHC class I, Tap proteins, and the transactivator Nlrc5, which is reversed upon stem cell entry into the cell cycle. These findings identify a link between tissue stem cell quiescence, antigen presentation, and immune evasion, and may help explain why mutations in long-lived stem cells would not lead to immune editing. They also suggest how cancer-initiating cells may evade immune surveillance

2018-04-01 | GSE109574 | GEO

MYC favors the onset of tumorigenesis by inducing epigenetic reprogramming of mammary epithelial cells towards a stem cell-like state [microarray]

Project description:We address the molecular mechanisms through which MYC promotes loss of cell identity and acquisition of stem cell-like traits, favouring the onset of tumorigenesis, by performing gene expression profile analyses in a transition from WT IMEC, IMEC over-expressing MYC and mammospeheres formed from IMEC-MYC (named M2). We then investigated the global gene expression profile of the fraction of cells hyper-activating the WNT pathway in M2 spheres, compared to the ones with low activation

2018-01-30 | GSE86407 | GEO

HBV suppresses expression of MICA/B on hepatoma cells through up-regulation of transcription factors GATA2 and GATA3 to escape from NK cell surveillance.

Project description:Decreased expression of NKG2D ligands on HBV-infected human hepatoma cells impairs NK cells lysis. However, which components of HBV exert this effect and the precise mechanisms need to be further investigated. In the present study, we observed that the HBx and HBc genes significantly down-regulated MICA expression. Through analysis with the chromatin immunoprecipitation assay, we found that HBV infection promotes the expression of transcription factors GATA-2 and GATA-3, which specifically suppressed MICA/B expression by directly binding to the promoter region of MICA/B. HBx protein, acting as a co-regulator, forms a tripolymer with GATA2 and GATA3, thus promotes the GATA-2 or GATA-3-mediated of MICA/B suppression. HBc protein inhibits MICA/B expression via directly binding to the CpG island in the MICA/B promoter. Thus, our study identified the novel role of transcription factors GATA-2 and GATA-3 in suppressing MICA/B expression and clarified the mechanisms of HBx and HBc in downregulation of MICA/B expression. These findings provide novel mechanisms for the contribution of HBV to hepatoma cells escape from NK cell surveillance.

| S-EPMC5302899 | biostudies-other

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