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HFD activated FAO mediates intestinal stemness and tumorgenicity I

ABSTRACT: HFD activated FAO mediates intestinal stemness and tumorgenicity I

PROVIDER: PRJNA634508 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11830314.fastq.gz	Fastqsanger.gz
	SRR11830315.fastq.gz	Fastqsanger.gz
	SRR11830316.fastq.gz	Fastqsanger.gz
	SRR11830317.fastq.gz	Fastqsanger.gz
	SRR11830318.fastq.gz	Fastqsanger.gz

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HFD activated FAO mediates intestinal stemness and tumorgenicity

Project description:HFD activated FAO mediates intestinal stemness and tumorgenicity

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HFD activated FAO mediates intestinal stemness and tumorgenicity II

Project description:HFD activated FAO mediates intestinal stemness and tumorgenicity II

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HFD activated FAO mediates intestinal stemness and tumorgenicity II

Project description:Obesity is an established risk factor for cancer in many tissues such as the gastrointestinal tract. In the mammalian intestine, a pro-obesity high fat diet (HFD) promotes tumorigenesis in part by enhancing intestinal stem cell (ISC) numbers, proliferation and function. Although Ppar (Peroxisome proliferator-activated receptor) nuclear receptor activity has been proposed to mediate some of these effects in HFD ISCs, the exact role that different Ppar family members play in this process is unclear. Here, we find that in loss-of-function in vivo models, both Ppar family members alpha and delta contribute to the HFD response in ISCs. Mechanistically, both PPARs do so by robustly inducing a downstream fatty acid oxidation (FAO) metabolic program. Notably, pharmacologic and genetic disruption of CPT1a (the rate limiting enzyme of FAO) blunts the HFD phenotype in ISCs. Furthermore, just as HFD ISCs depend on CPT1a-mediated FAO, inhibition of CPT1a dampens the pro-tumorigenic consequences of a HFD on early tumor incidence and progression in the intestine. These findings demonstrate that inhibition of a HFD activated FAO program creates a therapeutic opportunity to counter the effects of a HFD on ISCs and intestinal tumorigenesis.

2021-06-01 | GSE151046 | GEO

HFD activated FAO mediates intestinal stemness and tumorgenicity I

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HFD activated FAO mediates intestinal stemness and tumorgenicity

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

2021-06-01 | GSE151047 | GEO

High-fat diet activated fatty acid oxidation mediates intestinal stemness and tumorigenicity

2021-06-01 | GSE167996 | GEO

High-fat diet activated fatty acid oxidation mediates intestinal stemness and tumorigenicity

Project description:High-fat diet activated fatty acid oxidation mediates intestinal stemness and tumorigenicity

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High-fat diet activated fatty acid oxidation mediates intestinal stemness and tumorigenicity

Project description:High-fat diet activated fatty acid oxidation mediates intestinal stemness and tumorigenicity

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High-fat diet-activated fatty acid oxidation mediates intestinal stemness and tumorigenicity.

Project description:Obesity is an established risk factor for cancer in many tissues. In the mammalian intestine, a pro-obesity high-fat diet (HFD) promotes regeneration and tumorigenesis by enhancing intestinal stem cell (ISC) numbers, proliferation, and function. Although PPAR (peroxisome proliferator-activated receptor) nuclear receptor activity has been proposed to facilitate these effects, their exact role is unclear. Here we find that, in loss-of-function in vivo models, PPARα and PPARδ contribute to the HFD response in ISCs. Mechanistically, both PPARs do so by robustly inducing a downstream fatty acid oxidation (FAO) metabolic program. Pharmacologic and genetic disruption of CPT1A (the rate-controlling enzyme of mitochondrial FAO) blunts the HFD phenotype in ISCs. Furthermore, inhibition of CPT1A dampens the pro-tumorigenic consequences of a HFD on early tumor incidence and progression. These findings demonstrate that inhibition of a HFD-activated FAO program creates a therapeutic opportunity to counter the effects of a HFD on ISCs and intestinal tumorigenesis.

| S-EPMC8258630 | biostudies-literature

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.

2016-02-16 | E-GEOD-67324 | biostudies-arrayexpress

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