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Loss of Apc impairs Lgr5+ intestinal stem cell fate programs [RNA-seq]

ABSTRACT: Loss of Apc impairs Lgr5+ intestinal stem cell fate programs [RNA-seq]

PROVIDER: PRJNA507236 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8248770.fastq.gz	Fastqsanger.gz
	SRR8248771.fastq.gz	Fastqsanger.gz
	SRR8248762.fastq.gz	Fastqsanger.gz
	SRR8248772.fastq.gz	Fastqsanger.gz
	SRR8248763.fastq.gz	Fastqsanger.gz

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Loss of Apc impairs Lgr5+ intestinal stem cell fate programs

Project description:Loss of Apc impairs Lgr5+ intestinal stem cell fate programs

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Loss of Apc impairs Lgr5+ intestinal stem cell fate programs [RRBS]

Project description:Loss of Apc impairs Lgr5+ intestinal stem cell fate programs [RRBS]

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Loss of Apc impairs Lgr5+ intestinal stem cell fate programs [RRBS]

Project description:Loss of APC is the main driving alteration associated with colorectal cancer (CRC) development. We investigate the immediate outcome of this genetic event on the transcriptomic and DNA methylation profiles of Lgr5+ intestinal stem cells (ISCs), considered as the cell-of-origin of CRC. RNA-seq analyses show that the sequential deletion of Apc alleles has a rapid impact on the transcriptional profiles of ISCs. Indeed, Apc loss-of-function dictates an altered cell fate program at transcriptional level, resuting in an impaired commitment of those cells to differentiation. Reduced-representation bisufite sequencing (RRBS) on the genomic DNA (gDNA) also shows that focal alterations occur in the DNA methylations profiles of ISCs at this stage, and functionally contribute to altered cell fate in those cells. This study sheds light on the earliest events in CRC development, proving evidences on the role exerted by DNA methylation changes associated with Apc inactivation in the homeostatic rupture at CRC initation.

2020-03-22 | GSE123004 | GEO

Loss of Apc impairs Lgr5+ intestinal stem cell fate programs [RNA-seq]

2020-03-22 | GSE123005 | GEO

Loss of Apc impairs Lgr5+ intestinal stem cell fate programs

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

2020-03-22 | GSE123006 | GEO

Depletion of Apc gene in Cdx2 Gastro ntestinal Cells Facilitates Metastasis of Colorectal Adenocarcinoma Lgr5 Cells to Distant Organs

Project description:Caudal type homeobox 2 (CDX2) is a transcription factor expressed in the gastrointestinal (GI) epithelial (IEC) and stromal cells .CDX2 along with APC can regulate Lgr5 intestinal stem cell (ISC) differentiation to control GI tract development or intestinal neoplasia. CDX2 or APC loss function is associated with colorectal cancer (CRC) advance. However, whether APC directly regulates CRC metastasis is not clear. We aim to determine the role of inactive Apc gene in Cdx2 GI cells on Lgr5 ISC metastasis.

2025-03-03 | GSE226641 | GEO

Telomere Shortening Impairs PGC Fate Decision

Project description:Telomere Shortening Impairs PGC Fate Decision

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Gene expression profiles of DLD1 cells in which GATA6 or LGR5 expression was suppressed.

Project description:Mutations in APC or β-catenin that cause aberrant activation of Wnt signaling are responsible for the initiation of colorectal tumor development. LGR5 is specifically expressed in stem cells of the intestine, stomach and hair follicle, and plays essential roles in maintaining tissue homeostasis. LGR5-positive stem cells have been shown to be responsible for the intestinal adenoma initiated by some mutations in APC . Furthermore, it has recently been reported that Lgr5, which is associated with the Frizzled/Lrp Wnt receptor complex, interacts with R-spondins and thereby activates Wnt signaling. However, the function of LGR5 in colorectal tumorigenesis has been unclear. Here we show that LGR5 is required for the tumorigenicity of colorectal cancer cells. We also show that the transcription factor GATA6 directly enhances the expression of LGR5. DLD1 cells were infected with a lentivirus expressing an shRNA targeting GATA6 or LGR5.

2011-10-17 | E-GEOD-32987 | biostudies-arrayexpress

Apc-mutants act as supercompetitors in intestinal tumour initiation

Project description:Almost all colorectal cancers (CRC) present with mutations in the Apc gene, leading to unrestrained Wnt activation and the initiation of tumour development. We previously reported the competitive benefit of Apc-mutant intestinal stem cells (ISCs) within the crypt, however, the mechanism by which they outcompete their wild type (WT) neighbours remained elusive. Here, we studied the effect of Apc-mutants using an in vitro culture system of WT (Lgr5-CreErt2) and Apc-/- (Lgr5-CreErt2;Apcfl/fl) organoids . The expression patterns of WT and Apc-/- organoids revealed significant upregulation in specific secreted Wnt antagonists Notum, Wif1 and Dkk2. Furthermore, we studied the effect of the secreted antagonist by treating WT organoids with either WT or Apc-/- conditioned medium (CM) for 48 hours and observed a significant decrease in stem cell markers and an increase in goblet cell markers. We report that Apc-mutants act as bona fide supercompetitors by secreting Wnt antagonists that result in active differentiation of WT ISCs.

2021-03-25 | GSE144325 | GEO

Gene expression profiles of DLD1 cells in which GATA6 or LGR5 expression was suppressed.

2011-10-18 | GSE32987 | GEO