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Hypoxia limits the tumor-suppressive effects of C/EBPδ in pancreatic cancer

ABSTRACT: Hypoxia limits the tumor-suppressive effects of C/EBPδ in pancreatic cancer

PROVIDER: PRJNA938416 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23610780_1.fastq.gz	Fastqsanger.gz
	SRR23610780_2.fastq.gz	Fastqsanger.gz
	SRR23610781_1.fastq.gz	Fastqsanger.gz
	SRR23610781_2.fastq.gz	Fastqsanger.gz
	SRR23610782_1.fastq.gz	Fastqsanger.gz

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Hypoxia limits the tumor-suppressive effects of C/EBPδ in pancreatic cancer

Project description:Pancreatic ductal adenocarcinoma (PDAC) is a horrid disease with a terrifyingly low 5- year survival rate of only 12%. While this rate has slightly increased over the past decade, the incidence of PDAC has risen faster, by about 1% every year. Pre-clinical models are being employed with the aim to better understand the underlying tumor biology but sadly, a translation into the clinic often fails due to unforeseen complications. In a previous study, we showed that the transcription factor C/EBPδ has tumor-suppressive effects on PDAC cells in vitro. In this study, we take those findings a step further and assess the effect of C/EBPδ in a preclinical PDAC model in mice. We establish that the lack of oxygen in vivo – hypoxia - counteracts the tumor-suppressive effects of C/EBPδ in PDAC cells and suggest that this is partly mediated by a reciprocal feedback loop between C/EBPδ and HIF-1α. Although RNA-sequencing shows that the tumor-suppressive effects of C/EBPδ are not entirely abrogated under hypoxia, our study demonstrates the importance of considering major physiological parameters in order to make clinically relevant propositions.

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Pediatric AML classification according to C/EBPδ expression

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C/EBPδ drives key endocrine signals in human fetal membranes at parturition

Project description:Amnion-derived prostaglandin E2 (PGE2) and cortisol are key to labor onset. Identification of the common transcription factor driving the expression of both cyclooxygenase-2 (COX-2) and 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1), the key enzymes in their production, may hold the key to the treatment of pre- and post-term labor. Here, we have found that the CCAAT enhancer binding protein δ (C/EBPδ) is such a transcription factor which underlies the feed-forward induction of COX-2 and 11β-HSD1 expression by their own products PGE2 and cortisol in human amnion fibroblasts so that their production would be ensured in the amnion for the onset of labor. Moreover, the abundance of C/EBPδ in amnion increases along with COX-2 and 11β-HSD1 at term and further increases at parturition. Knockout of C/EBPδ in mice delays the onset of labor further supporting the concept. In conclusion, C/EBPδ may serve as a novel pharmaceutical target in the amnion for treatment of pre- and post-term labor.

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Project description:Pancreatic ductal adenocarcinoma (PDAC) is characterized by an extensive fibroinflammatory stromal reaction, which contributes to its hypovascular and hypoxic microenvironment. To assess the effects of hypoxia on fibroblast phenotype in an unbiased fashion, we performed RNA-sequencing profiling of mouse pancreatic stellate cells (PSCs) cocultured with mT3 PDAC cells exposed to normoxia (21% oxygen) or hypoxia (1% oxygen).

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C/EBPδ drives key endocrine signals in human fetal membranes at parturition [ChIP-seq]

Project description:Amnion-derived prostaglandin E2 (PGE2) and cortisol are key to labor onset. Identification of the common transcription factor driving the expression of both cyclooxygenase-2 (COX-2) and 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1), the key enzymes in their production, may hold the key to the treatment of pre- and post-term labor. Here, we have found that the CCAAT enhancer binding protein δ (C/EBPδ)is such a transcription factor which underlies the feed-forward induction of COX-2 and 11β-HSD1 expression by their own products PGE2 and cortisol in human amnion fibroblasts so that their production would be ensured in the amnion for the onset of labor. Moreover, the abundance of C/EBPδin amnion increases along with COX-2 and 11β-HSD1 at term and further increases at parturition. Knockout of C/EBPδ in mice delays the onset of labor further supporting the concept. In conclusion, C/EBPδmay serve as a novel pharmaceutical target in the amnion for treatment of pre- and post-term labor.

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