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The CDP-Etn pathway accelerates mesenchymal-to-epithelial transition in somatic cell reprogramming

ABSTRACT: the CDP-Etn pathway accelerates mesenchymal-to-epithelial transition in somatic cell reprogramming

PROVIDER: PRJNA476964 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7405190_1.fastq.gz	Fastqsanger.gz
	SRR7405190_2.fastq.gz	Fastqsanger.gz
	SRR7405191_1.fastq.gz	Fastqsanger.gz
	SRR7405191_2.fastq.gz	Fastqsanger.gz
	SRR7405186_1.fastq.gz	Fastqsanger.gz

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the CDP-Etn pathway accelerates mesenchymal-to-epithelial transition in somatic cell reprogramming

Project description:Metabolic reprogramming has emerged as key regulators of cell fate decisions. Whereas the glucose and amino acid metabolism have been extensively documented, the roles of lipid metabolism in pluripotency remain largely unexplored. Here, we report that the CDP-Ethanolamine (CDP-Etn) pathway for phosphatidylethanolamine synthesis is required for somatic cell reprogramming at the early stage. Mechanistically, the CDP-Etn pathway inhibits NF-κB signaling and mesenchymal genes in a Pebp1 dependent manner, resulting in accelerated mesenchymal-to-epithelial transition and enhanced reprogramming. In addition, we show that phospholipids are critical for the growth of mESC though without effects on pluripotency. Our study reveals an unforeseen connection between phospholipids, cell migration and pluripotency and highlights the importance of phospholipids in cell fate transitions.

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Loss of ATM accelerates pancreatic cancer formation and epithelial–mesenchymal transition

Project description:Pancreatic ductal adenocarcinoma (PDAC) is associated with accumulation of particular oncogenic mutations and recent genetic sequencing studies have identified ataxia telangiectasia-mutated (ATM) mutations in PDAC cohorts. Here we report that conditional deletion of ATM in a mouse model of PDAC induces a greater number of proliferative precursor lesions coupled with a pronounced fibrotic reaction. ATM-targeted mice display altered TGFβ-superfamily signalling and enhanced epithelial-to-mesenchymal transition (EMT) coupled with shortened survival. Notably, our mouse model recapitulates many features of more aggressive human PDAC subtypes. Particularly, we report that low expression of ATM predicts EMT, a gene signature specific for Bmp4 signalling and poor prognosis in human PDAC. Our data suggest an intimate link between ATM expression and pancreatic cancer progression in mice and men. KC (Atm+/+) and AKC (Atm-/-) mouse pancreata at 5 weeks old (n= 3 KC; n= 3 AKC) or 10 weeks old (n=3 KC; n=4 AKC) were subjected to microarray analysis.

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Oocyte Specific Homeobox 1 (Obox1) Facilitates Somatic Cell Reprogramming by Promoting Mesenchymal-to-Epithelial Transition and Mitigating Cell Hyper-proliferation

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