Ontology highlight
ABSTRACT:
PROVIDER: PRJNA997814 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25394400.fastq.gz | Fastqsanger.gz | |||
| SRR25394401.fastq.gz | Fastqsanger.gz | |||
| SRR25394386.fastq.gz | Fastqsanger.gz | |||
| SRR25394387.fastq.gz | Fastqsanger.gz | |||
| SRR25394388.fastq.gz | Fastqsanger.gz |
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Project description:To further elucidate the role of the intestinal stem cell marker Leucine-rich-repeat-containing G-protein-coupled receptor 5 (LGR5) in colorectal cancer (CRC), we exposed Lgr5-EGFP-IRES-Cre-ERT2 mice to azoxymethane/dextrane sodium sulfate (AOM/DSS) which induces inflammation-driven colon tumors. Tumors were then flow-sorted into fractions of epithelial cells that expressed high or low levels of Lgr5 and were characterized using gene expression profiling. In the AOM/DSS-induced mouse colon tumors Lgr5 high cells showed higher levels of several stem cell-associated genes and higher Wnt signaling than Lgr5 low tumor cells and Lgr5 high normal colon epithelial cells. To further elucidate the role of the intestinal stem cell marker Leucine-rich-repeat-containing G-protein-coupled receptor 5 (LGR5) in colorectal cancer (CRC), we transduced SW480 CRC cells with lentiviral shRNA constructs to silence LGR5 expression. This resulted in a depletion of spheres but did not affect adherently growing cells. Spheres expressed higher levels of several stem cell-associated genes than adherent cells. Notch signaling was down-regulated upon LGR5 silencing. This was confirmed by immunohistochemistry against cleaved NOTCH1.
2013-04-19 | GSE46200 | GEO
Project description:To further elucidate the role of the intestinal stem cell marker Leucine-rich-repeat-containing G-protein-coupled receptor 5 (LGR5) in colorectal cancer (CRC), we exposed Lgr5-EGFP-IRES-Cre-ERT2 mice to azoxymethane/dextrane sodium sulfate (AOM/DSS) which induces inflammation-driven colon tumors. Tumors were then flow-sorted into fractions of epithelial cells that expressed high or low levels of Lgr5 and were characterized using gene expression profiling. In the AOM/DSS-induced mouse colon tumors Lgr5 high cells showed higher levels of several stem cell-associated genes and higher Wnt signaling than Lgr5 low tumor cells and Lgr5 high normal colon epithelial cells. To further elucidate the role of the intestinal stem cell marker Leucine-rich-repeat-containing G-protein-coupled receptor 5 (LGR5) in colorectal cancer (CRC), we transduced SW480 CRC cells with lentiviral shRNA constructs to silence LGR5 expression. This resulted in a depletion of spheres but did not affect adherently growing cells. Spheres expressed higher levels of several stem cell-associated genes than adherent cells. Notch signaling was down-regulated upon LGR5 silencing. This was confirmed by immunohistochemistry against cleaved NOTCH1. Normal mouse colons and AOM/DSS-induced mouse colon tumors were flow-sorted into Lgr5 high and low cells before gene expression was measured. Fifteen independent experiments were performed using seven individual mice for normal colons and eight for tumors. Appropriate LGR5 status was confirmed by real-time qRT-PCR before measuring silencing induced gene expression. Three independent experiments were performed for each cell fraction using separately cultured cells for each experiment.
2013-04-19 | E-GEOD-46200 | biostudies-arrayexpress
Project description:This study aims to determine the safety and best response of treatment with CNA3103 (Leucine-rich repeat-containing G protein-coupled receptor 5 [LGR5]-targeted, Autologous Chimeric Antigen Receptor (CAR) -T Cells), for participants with Metastatic Colorectal Cancer.
Participants may undergo a pre-screening biopsy procedure to determine expression of LGR5.
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Project description:The molecular mechanisms controlling stem cell renewal and lineage commitment are still poorly understood due to lack of reliable markers. In the adult small intestine, an example of high rate self-renewing tissue, four different epithelial cell lineages (enterocytes, Goblet, enteroendocrine and Paneth cells) are generated from a pool of stem cells localised at the bottom of the crypts of Lieberkühn. Recently, the orphan Leucine-rich repeat G protein-coupled receptor 5 (GPR49), a target of Wnt signalling, has been proposed as a marker for such cells. We investigated the role of LGR5 during intestinal development by using LGR5 null/LacZ-NeoR knock-in mice. We show that LGR5 deficiency leads to premature Paneth cell differentiation. X-gal staining on E18.5 intestine revealed that LGR5 expression is restricted to a few cells clustered within the intervillus region known to contain progenitor cells. In LGR5-null mice, expression from the LGR5 promoter was found upregulated, suggesting a loss of negative feedback control. However, neither epithelial cell proliferation nor cell migration appeared significantly impaired by LGR5 deficiency. Finally, transcriptional profiling of ileal mutant mice suggests that LGR5 plays a role in regulating the Wnt and Notch signalling pathways controlling progenitor renewal and differentiation.
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Project description:Inhibition of leucine-rich repeat-containing G protein-coupled receptor 4 (Lgr4) prevents the development of Mixed Lineage Leukemia (MLL)-arranged AML in mice and suppresses activation of Wnt/beta-catenin signaling. To identify key downstream targets of Lgr4, we performed genome-wide gene expression analysis. Our microarray analysis and subsequent in vivo studies demonstrate a novel functional role for growth arrest and DNA damage-inducible 45 (Gadd45a) in promoting in vivo self-renewal of leukemic stem cells in MLL-rearranged AML. GFP-positive leukemic cells flow-sorted by BD Influx cell sorter from bone marrow of primary AML mice induced by MLL-AF9 oncogene were lentivirally transduced with Lgr4 shRNA (MSH040504-3-LVRU6MP, GeneCopoeia) or Scrambled control (CSHCTR001-LVRU6MP, GeneCopoeia), and replated in methylcellulose supplemented with IL3. Each group contains triplicate samples.
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Project description:Progeny from a cross of Arabidopsis thaliana Landsberg (Ler, Poland) and Kashmir-2 (Kas-2, central Asia) accessions exhibit immune-related hybrid incompatibility (HI) due to a genetic interaction between a cluster of eight TNL (Toll/Interleukin1 Receptor- Nucleotide Binding - Leucine Rich Repeat) RPP1-like (Recognition of Peronospora parasitica 1-like) genes (R1- R8) from Ler and central Asian alleles of a Strubbelig-family receptor-like kinase (SRF3). In characterizing mutants altered in Ler/Kas-2 HI, we mapped multiple intragenic mutations to the RPP1-like Ler locus. The expression of sulki1 (suppressor of Ler/Kas-2 incompatibility 1) mutant mapping to RPP1-like R8 Ler, the parental line Kas-2 accession and the Ler/Kas-2 NIL have been determined by RNA-seq in 5-week old plants grown at 14 - 16 ºC.
2018-05-16 | E-MTAB-6755 | biostudies-arrayexpress
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