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Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors.

ABSTRACT: Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors.

PROVIDER: PRJNA779920 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16928930_1.fastq.gz	Fastqsanger.gz
	SRR16928930_2.fastq.gz	Fastqsanger.gz
	SRR16928931_1.fastq.gz	Fastqsanger.gz
	SRR16928931_2.fastq.gz	Fastqsanger.gz
	SRR16928932_1.fastq.gz	Fastqsanger.gz

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Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors [bulk RNA-Seq]

Project description:Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors [bulk RNA-Seq]

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Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors [bulk RNA-Seq]

Project description:Cancers of the gastrointestinal tract including esophageal adenocarcinomas, colorectal cancers, and cancers of the gastric cardia are common comorbidities of obesity. Excessive delivery of macronutrients to the cells lining the gut can increase one’s risk for these cancer by inducing imbalances in the rate of intestinal stem cell proliferation vs. differentiation, which can produce polyps and other aberrant growths. We demonstrate that serine palmitoyltransferase (SPT), which diverts dietary fatty and amino acids into the sphingolipid biosynthesis pathway, is a critical modulator of intestinal stem cell homeostasis. SPT and other enzymes in the biosynthetic pathway are upregulated in human colon tumors. These enzymes produce sphingolipids that serve as pro-stemness signals that stimulate peroxisome-proliferator activated receptor alpha (PPARa)-mediated induction of fatty acid binding protein-1. This increases fatty acid uptake and oxidation and enhances the stemness program. Serine palmitoyltransferase thus serves as a critical link between dietary macronutrients, epithelial regeneration, and cancer risk.

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Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors [single cell RNA-Seq]

Project description:Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors [single cell RNA-Seq]

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Serine Palmitoyltransferase Controls Stemness of Intestinal Progenitors.

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

2022-11-01 | GSE188676 | GEO

Yeast Serine palmitoyl transferase interaction proteomics

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High-fat diet enhances stemness and tumorigenicity of intestinal progenitors

Project description:Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we find that high fat diet (HFD)-induced obesity augments the numbers and function of Lgr5+ intestinal stem cells (ISCs) of the mammalian intestine. Like HFD, ex vivo treatment of intestinal organoid cultures with palmitic acid (PA), a constituent of the HFD, enhances the self-renewal potential of these organoid bodies. Mechanistically, HFD induces a robust peroxisome proliferator-activated receptor delta (PPAR-delta signature in intestinal stem and progenitor cells and pharmacologic activation of PPAR-delta recapitulates the effects that HFD has on these cells. Interestingly, HFD- and agonist-activated PPAR-delta signaling endows organoid-initiating capacity to non-stem cells and enforced PPAR-delta signaling permits these non-stem cells to form in vivo tumors upon loss of the tumor suppressor Apc. These findings highlight how diet-modulated PPAR-delta activation alters not only the function of intestinal stem and progenitor cells but also their capacity to initiate tumors. mRNA profiles of intestinal stem cells (GFP-Hi) and progenitors (GFP-Low) from WT or HFD fed mice were generated by deep sequencing using HiSeq 2000.

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Effect of D-serine on gene expression in Neuro2a cells

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High-fat diet enhances stemness and tumorigenicity of intestinal progenitors.

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| S-EPMC4846772 | biostudies-literature

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