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Interferon-gamma is Quintessential for NOS2 and COX2 Expression in ER- Breast Tumors that Lead to Poor Outcome

ABSTRACT: Interferon-gamma is Quintessential for NOS2 and COX2 Expression in ER- Breast Tumors that Lead to Poor Outcome

PROVIDER: PRJNA972735 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24572316.fastq.gz	Fastqsanger.gz
	SRR24572317.fastq.gz	Fastqsanger.gz
	SRR24572318.fastq.gz	Fastqsanger.gz
	SRR24572319.fastq.gz	Fastqsanger.gz
	SRR24572320.fastq.gz	Fastqsanger.gz

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Interferon-gamma is Quintessential for NOS2 and COX2 Expression in ER- Breast Tumors that Lead to Poor Outcome

Project description:Previously, we have proved the NOS2 and COX2 genes play an important role in ER-negative breast cancer. In this study, we utilized the scRNAseq technique to investigate how cancer cells react to cytokines with and without IFNG combination treatments.

2023-12-31 | GSE232567 | GEO

Interferon-gamma is quintessential for NOS2 and COX2 expression in ER<sup>-</sup> breast tumors that lead to poor outcome.

Project description:A strong correlation between NOS2 and COX2 tumor expression and poor clinical outcomes in ER breast cancer has been established. However, the mechanisms of tumor induction of these enzymes are unclear. Analysis of The Cancer Genome Atlas (TCGA) revealed correlations between NOS2 and COX2 expression and Th1 cytokines. Herein, single-cell RNAseq analysis of TNBC cells shows potent NOS2 and COX2 induction by IFNγ combined with IL1β or TNFα. Given that IFNγ is secreted by cytolytic lymphocytes, which improve clinical outcomes, this role of IFNγ presents a dichotomy. To explore this conundrum, tumor NOS2, COX2, and CD8+ T cells were spatially analyzed in aggressive ER-, TNBC, and HER2 + breast tumors. High expression and clustering of NOS2-expressing tumor cells occurred at the tumor/stroma interface in the presence of stroma-restricted CD8+ T cells. High expression and clustering of COX2-expressing tumor cells extended into immune desert regions in the tumor core where CD8+ T cell penetration was limited or absent. Moreover, high NOS2-expressing tumor cells were proximal to areas with increased satellitosis, suggestive of cell clusters with a higher metastatic potential. Further in vitro experiments revealed that IFNγ + IL1β/TNFα increased the elongation and migration of treated tumor cells. This spatial analysis of the tumor microenvironment provides important insight into distinct neighborhoods where stroma-restricted CD8+ T cells exist proximal to NOS2-expressing tumor niches that could have increased metastatic potential.

| S-EPMC10175544 | biostudies-literature

Ptch1+/- Nos2-/- medulloblastomas

Project description:This SuperSeries is composed of the following subset Series: GSE29192: Implication of Nos2 inactivation on the transcriptome of developing cerebellum and Ptch1+/- medulloblastomas (mRNA) GSE29199: Implication of Nos2 inactivation on genomic changes in Ptch1+/- medulloblastomas (array-CGH) Refer to individual Series

2011-12-01 | E-GEOD-29201 | biostudies-arrayexpress

Expression data from targeting of NOS2 in glioma stem cells

Project description:Analysis of the effects of targeting NOS2 at the gene expression level. Our studies demonstrated a role for NOS2 in glioma biology through the maintenance of the glioma stem cell phenotype. Microarray results provide novel targets of NOS2 and suggest mechanisms through which NOS2 contributes to glioma stem cell biology. Glioma stem cells isolated from two different human glioma xenografts were infected with a non-targeting control shRNA or two different shRNAs directed against NOS2 (each treatment in each tumor performed in technical duplicates).

2011-07-08 | E-GEOD-29750 | biostudies-arrayexpress

Expression data from targeting of NOS2 in glioma stem cells

2011-07-08 | GSE29750 | GEO

Expression data from from NOS2-deficient (NOS2-/-) and wild-type mice subjected to endotoxin or saline challenge

Project description:Hypoxic pulmonary vasoconstriction (HPV) optimizes the match between ventilation and perfusion in the lung by reducing blood flow to poorly ventilated regions. Sepsis and endotoxemia impair HPV. We previously showed that nitric oxide synthase 2 (NOS2) is required, but not sufficient, for the effect of endotoxin on HPV. The aim of the current study was to identify additional factors that might contribute to the impairment of HPV during endotoxemia. Microarray gene expression profiling was determined using pulmonary tissues from NOS2-deficient (NOS2-/-) and wild-type mice subjected to endotoxin (LPS) or saline challenge (control).

2019-05-09 | GSE130936 | GEO

Association of microRNAs with CD68 and NOS2 in IBD tissues.

Project description:We analyzed the association of CD68 and NOS2 mRNA expression with microRNAs in IBD tissues. For this analysis, data was LOESS normalized in R. Data was then imported into Partek Genomics Suite and Batch effects caused by day to day variability (Dategroup of array charateristic) were corrected. We did not have mRNA expression data for CD68 and NOS2 for all of the samples, therefore those samples were not used for analysis. We identified several microRNAs associated with CD68 and NOS2 expression. Total mRNA was extracted from colon tissue that was flash frozen immediately after surgery. A total of 114 tissues were used for microarray analysis. Briefly, 5 ug of RNA were biotin labeled and hybridized to OSU-CCC microRNA microarrays version 2.0. We then analyzed associations with CD68 and NOS2 mRNA expression.

2012-07-31 | E-GEOD-29703 | biostudies-arrayexpress

Association of microRNAs with CD68 and NOS2 in IBD tissues.

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Tristetraprolin targets Nos2 expression in the colonic epithelium

Project description:Tristetraprolin (TTP), encoded by the Zfp36 gene, is a zinc-finger protein that regulates RNA stability primarily through association with 3’ untranslated regions (3’UTRs) of target mRNAs. While TTP is expressed abundantly in the intestines, its function in intestinal epithelial cells (IECs) is unknown. Here we used a cre-lox system to remove Zfp36 in the mouse epithelium to uncover a role for TTP in IECs and to identify target genes in these cells. While TTP was largely dispensable for establishment and maintenance of the colonic epithelium, we found an expansion of the proliferative zone and an increase in goblet cell numbers in the colon crypts of Zfp36ΔIEC mice. Furthermore, through RNA-sequencing of transcripts isolated from the colons of Zfp36fl/fl and Zfp36ΔIEC mice, we found that expression of inducible nitric oxide synthase (iNos or Nos2) was elevated in TTP-knockout IECs. We demonstrate that TTP interacts with AU-rich elements in the Nos2 3’UTR and suppresses Nos2 expression. In comparison to control Zfp36fl/fl mice, Zfp36ΔIEC mice were less susceptible to dextran sodium sulfate (DSS)-induced acute colitis. Together, these results demonstrate that TTP targets Nos2 expression in IECs and aggravates acute colitis.

2019-12-04 | GSE123345 | GEO

Implication of Nos2 inactivation on genomic changes in Ptch1+/- medulloblastomas (array-CGH)

Project description:The Ptch1+/- strain constitues an established mouse model for the Shh-driven type of medulloblastoma. Combined Ptch1+/- Nos2-/- mice show a two-fold increased incidence for this tumor. Here, the impact of Nos2 inactivation on copy number alterations during medulloblastoma development was investigated by array-based comparative genomic hybridization (arrayCGH) of tumor samples from both genotypes. Medulloblastoma samples from five Ptch1+/- and seven compound Ptch1+/- Nos2-/- mice were analyzed. Cy5-labeled tumor DNA was combined with corresponding Cy3-labeled reference healthy wildtype genomic DNA to receive either sex-matched sample pairs or pairs of different gender for internal negative or positive control.

2011-12-01 | E-GEOD-29199 | biostudies-arrayexpress

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