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Chronic Interferon Stimulated Gene Transcription Promotes Oncogene Induced Breast Cancer [RNA-Seq]

ABSTRACT: Chronic Interferon Stimulated Gene Transcription Promotes Oncogene Induced Breast Cancer [RNA-Seq]

PROVIDER: PRJNA1032887 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26549104_1.fastq.gz	Fastqsanger.gz
	SRR26549104_2.fastq.gz	Fastqsanger.gz
	SRR26549105_1.fastq.gz	Fastqsanger.gz
	SRR26549105_2.fastq.gz	Fastqsanger.gz
	SRR26549106_1.fastq.gz	Fastqsanger.gz

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Chronic Interferon Stimulated Gene Transcription Promotes Oncogene Induced Breast Cancer

Project description:Chronic Interferon Stimulated Gene Transcription Promotes Oncogene Induced Breast Cancer

| PRJNA1036222 | ENA

Chronic Interferon Stimulated Gene Transcription Promotes Oncogene Induced Breast Cancer [RNA-Seq]

Project description:The Mre11 complex (comprising Mre11, Rad50, Nbs1) is integral to the maintenance of genome stability. We previously showed that a hypomorphic Mre11 mutant mouse strain (Mre11ATLD1/ATLD1) was highly susceptible to oncogene induced breast cancer. Here we used a mammary organoid system to examine which Mre11 dependent responses are tumor suppressive. We found that Mre11ATLD1/ATLD1 organoids exhibited an elevated interferon stimulated gene (ISG) signature and sustained changes in chromatin accessibility. This Mre11ATLD1/ATLD1 phenotype depended on DNA binding of a nuclear innate immune sensor, IFI205. Ablation of Ifi205 in Mre11ATLD1/ATLD1 organoids restored baseline and oncogene-induced chromatin accessibility patterns to those observed in WT. Implantation of Mre11ATLD1/ATLD1 organoids and activation of oncogene led to aggressive metastatic breast cancer. This outcome was reversed in implanted Ifi205-/- Mre11ATLD1/ATLD1 organoids. These data reveal a connection between innate immune signaling and tumor suppression in mammary epithelium. Given the abundance of aberrant DNA structures that arise in the context of genome instability syndromes, the data further suggest that cancer predisposition in those contexts may be partially attributable to tonic innate immune transcriptional programs.

2024-12-18 | GSE246409 | GEO

Chronic Interferon Stimulated Gene Transcription Promotes Oncogene Induced Breast Cancer

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

2024-12-20 | GSE247101 | GEO

Interferon-stimulated gene expression in STAT1 knockout cells

2016-07-22 | GSE84693 | GEO

Interferon-stimulated gene expression in STAT1 knockout cells

Project description:STAT1 plays a cental role in the induction of interferon-stimulated genes, but interferon alpha can activate a STAT1-independent pathway that leads to gene expression. We performed microarray analysis to examine whether like interferon alpha, interferon lambda, a newly discovered interferon, can induce the expression of interferon-stimulated genes in the absence of STAT1. Control and STAT1 knockout Huh-7.5 hepatoma cells were left untreated or treated with 1000 U/ml of human interferon alpha 2a or interferon lambda 1 (PBL) for 24 h, and total RNA was extracted. Sense-strand DNA was generated from 200 ng of total RNA, fragmented, and labeled using a GeneChip WT Plus Reagent Kit (Affymetrix). Six samples were obtained and each sample was anlyzed using one GeneChip.

2016-07-22 | E-GEOD-84693 | biostudies-arrayexpress

Project description:Background: Hepatitis E Virus (HEV) is a new causative agent of chronic hepatitis in solid organ transplant recipients in Europe. Factors associated with the occurrence and persistence of chronic HEV infection remain largely unknown but chronic evolution seems to be the consequence of hostM-bM-^@M-^Ys immunological factors rather than of viral factors. Method: In a prospective case-control study, we have determined in whole blood of chronically HEV-infected kidney-transplant recipients the host response using microarray technology. Results: Chronically HEV-infected kidney-transplant recipients exhibited a specific transcriptional program, in which interferon effectors were prominent. The intensity of expression of each signatureM-bM-^@M-^Ys gene was significantly lower in patients who were subsequently cleared of HEV than in patients who were not. Furthermore, in patients who were cleared of HEV, a higher expression of these genes was associated with a longer delay until HEV clearance. Conclusions: The specific transcriptional program determined in chronically HEV-infected kidney-transplant recipients suggests an activation of type I interferon response. Intensity of interferon-stimulated genes expression could be useful to forecast the outcome of infection. High expression of interferon-stimulated genes could signify a dysregulation in the interferon response that might favour the persistence of the HEV infection. TrialM-bM-^@M-^Ys registration number: NCT01090232; RegistryM-bM-^@M-^Ys URL: http://clinicaltrials.gov/ct2/show/study/NCT01090232?term=kidney+transplant+recipients&cntry1=EU%3AFR&rank=2 Total RNA was extracted from whole-blood sample or monocytes of kidney-transplant patients with or without chronic hepatitis E (CHE) infection. Control patients were matched up with CHE patients for age, sex, time since kidney transplant and immunosuppressive treatment.

2013-01-29 | E-GEOD-36539 | biostudies-arrayexpress

Project description:Background: Hepatitis E Virus (HEV) is a new causative agent of chronic hepatitis in solid organ transplant recipients in Europe. Factors associated with the occurrence and persistence of chronic HEV infection remain largely unknown but chronic evolution seems to be the consequence of host’s immunological factors rather than of viral factors. Method: In a prospective case-control study, we have determined in whole blood of chronically HEV-infected kidney-transplant recipients the host response using microarray technology. Results: Chronically HEV-infected kidney-transplant recipients exhibited a specific transcriptional program, in which interferon effectors were prominent. The intensity of expression of each signature’s gene was significantly lower in patients who were subsequently cleared of HEV than in patients who were not. Furthermore, in patients who were cleared of HEV, a higher expression of these genes was associated with a longer delay until HEV clearance. Conclusions: The specific transcriptional program determined in chronically HEV-infected kidney-transplant recipients suggests an activation of type I interferon response. Intensity of interferon-stimulated genes expression could be useful to forecast the outcome of infection. High expression of interferon-stimulated genes could signify a dysregulation in the interferon response that might favour the persistence of the HEV infection. Trial’s registration number: NCT01090232; Registry’s URL: http://clinicaltrials.gov/ct2/show/study/NCT01090232?term=kidney+transplant+recipients&cntry1=EU%3AFR&rank=2

2013-01-29 | GSE36539 | GEO

Gene induction by the USP6 oncogene in response to interferon

Project description:Gene induction by the USP6 oncogene in response to interferon

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DLEU1 promotes oral squamous cell carcinoma progression through activating interferon-stimulated genes

Project description:DLEU1 promotes oral squamous cell carcinoma progression through activating interferon-stimulated genes

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Impact of ETV7 activity on interferon-stimulated gene expression in 293T cells treated with interferon alpha

Project description:293T cells constitutively expressing ETV7 have reduced expression of interferon-stimulated genes.

2019-11-21 | GSE140709 | GEO