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A Tumour-Resident Lgr5+ Stem Cell - Like Pool Drives the Establishment and Progression of Advanced Gastric Cancers

ABSTRACT: A Tumour-Resident Lgr5+ Stem Cell - Like Pool Drives the Establishment and Progression of Advanced Gastric Cancers

PROVIDER: PRJNA765365 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16013091_1.fastq.gz	Fastqsanger.gz
	SRR16013091_2.fastq.gz	Fastqsanger.gz
	SRR16013092_1.fastq.gz	Fastqsanger.gz
	SRR16013092_2.fastq.gz	Fastqsanger.gz
	SRR16013093_1.fastq.gz	Fastqsanger.gz

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A Tumour-Resident Lgr5+ Stem Cell - Like Pool Drives the Establishment and Progression of Advanced Gastric Cancers

Project description:Gastric cancer is amongst the most prevalent and deadliest cancers globally. To derive mechanistic insight into the pathways governing this disease, we generated a stomach-specific Claudin18-IRES-CreERT2 mouse line to model advanced human gastric cancer and investigated the role of tumour resident Lgr5+ stem-like cells in gastric cancer. Mouse lines incorporating Cldn18-driven conditional dysregulation of the Wnt, RTK and Trp53 pathways modelled metastatic Chromosomal Instable-type gastric cancer. In parallel, we supplemented these cancer models with orthotopic transplantation of cancer organoids to derive detailed mechanistic insight into the roles of Lgr5+ cancer stem cell in gastric cancer. Here we show, we recapitulated advanced human gastric cancer in terms of disease phenotype, aberrant gene expression profile, molecular markers, and sites of distant metastases. Importantly, we established that tumour-resident Lgr5+ stem-like cells are critical to the initiation and maintenance of tumour burden, and are obligatory for the establishment of metastases. These models will be invaluable for deriving clinically-relevant mechanistic insights into cancer progression and as pre-clinical models for evaluating novel therapeutics.

2021-11-26 | GSE184613 | GEO

A constant pool of Lgr5+ intestinal stem cells is required for intestinal homeostasis

Project description:Lgr5+ crypt base columnar cells, the operational intestinal stem cells (ISCs), are thought to be dispensable for small intestinal (SI) homeostasis. Using a novel Lgr5-2A-DTR (Diphtheria Toxin Receptor) model which ablates Lgr5+ cells with near-complete efficiency and retains endogenous levels of Lgr5 expression, we show that persistent depletion of Lgr5+ ISCs in fact compromises SI epithelial integrity and reduces epithelial turnover in vivo. In vitro, Lgr5-2A-DTR SI organoids are unable to establish or survive when Lgr5+ ISCs are continuously eliminated when DT is in the media. However, transient exposure to DT at the start of culture allows organoids to form, and the rate of outgrowth reduces with increasing length of DT presence. Our results indicate that intestinal homeostasis requires a constant pool of Lgr5+ ISCs, which is supplied by rapidly reprogrammed non-Lgr5+ crypt populations when pre-existing Lgr5+ ISCs are ablated.

2020-12-31 | GSE148727 | GEO

Expression data of GFP-high or low cells of LGR5-GFP or KRT20-GFP knock-in human colorectal tumor organoids.

Project description:We analyzed gene expression of 3 lines LGR5-GFP, 2 lines KRT20-GFP knock-in colorectal tumor organdies. The cancer stem cell (CSC) theory highlights a self-renewing subpopulation of cancer cells that fuels tumour growth. The existence of human CSCs is mainly supported by xenotransplantation of prospectively isolated cells, but their clonal dynamics and plasticity remain unclear. Here, we show that human LGR5+ colorectal cancer cells serve as CSCs in growing cancer tissues. Lineage-tracing experiments with a tamoxifen inducible Cre knock-in allele of LGR5 reveal the self-renewal and differentiation capacity of LGR5+ tumour cells. Selective ablation of LGR5+ CSCs in LGR5-iCaspase9 knock-in organoids leads to tumour regression, followed by tumour regrowth driven by re-emerging LGR5+ CSCs. KRT20 knock-in reporter marks differentiated cancer cells that constantly diminish in tumour tissues, while reverting to LGR5+ CSCs and contributing to tumour regrowth after LGR5+ CSC ablation. We also show that combined chemotherapy potentiates LGR5+ CSCs targeting. These data provide insights into the plasticity of CSCs and their potential as a therapeutic target in human colorectal cancer.

2017-03-30 | GSE83513 | GEO

A slow cycling Lgr5 tumour population mediates basal cell carcinoma relapse after therapy

Project description:A slow cycling Lgr5 tumour population mediates basal cell carcinoma relapse after therapy

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Methylation profiling blood, adjacent benign and multiple discrete tumour samples from locally advanced prostate cancers.

Project description:We systematically dissected prostetectamy samples from three men with locally advanced prostate cancer, isolating histologically benign tissue and spatially separated tumour samples. In total 24 samples (including blood samples) were profiled using Infinium HumanMethylation450k arrays.

2014-12-31 | E-MTAB-2964 | biostudies-arrayexpress

Lgr5+ stem and progenitor cells reside at the apex of a heterogeneous embryonic hepatoblast pool

Project description:During mouse embryogenesis, progenitors within the liver known as hepatoblasts give rise to adult hepatocytes and cholangiocytes. Hepatoblasts, which are specified at E8.5-E9.0, have been regarded as a homogeneous progenitor population that initiate differentiation from E13.5. Recently, scRNA-seq analysis has identified sub- populations of transcriptionally distinct hepatoblasts at E11.5. Here, we show that hepatoblasts are not only transcriptionally but also functionally heterogeneous, and that a subpopulation of E9.5-E10.0 hepatoblasts exhibit a previously unidentified early commitment to cholangiocyte fate. Importantly, we also identify a sub-population constituting 2% of E9.5-E10.0 hepatoblasts that express the adult stem cell marker Lgr5, and generate both hepatocyte and cholangiocyte progeny that persist for the lifespan of the mouse. Combining lineage tracing and scRNA-seq, we show that Lgr5 marks E9.5-E10.0 bipotent liver progenitors residing at the apex of a hepatoblast hierarchy. Notably, isolated Lgr5+ hepatoblasts can be clonally expanded in vitro into embryonic liver organoids, which can commit to either hepatocyte or cholangiocyte fates. Our study demonstrates functional heterogeneity within E9.5 hepatoblasts and identifies Lgr5 as a marker for a sub-population of bipotent liver progenitors.

2019-05-27 | GSE123103 | GEO

The role of Lgr5 intestinal cancer stem cells in tumour initiation, progression and metastasis

Project description:The role of Lgr5 intestinal cancer stem cells in tumour initiation, progression and metastasis

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Gastric squamous-columnar junction contains a large pool of cancer-prone immature osteopontin responsive Lgr5-CD44+ cells

Project description:We report the gene expression profiles of gastric squamous-columnar junction cancer derived from the mice with conditionally inactivation of Trp53 and Rb1 genes in Lgr5+ cells

2020-01-13 | GSE130003 | GEO

Lgr5+tuft marker+ intestinal tumor cells

Project description:We previously identified Dclk1, a tuft cell marker, marks tumor stem cells (TSCs) in mouse intestinal tumors. In this study, we have identified IL17RB as a cell surface marker distinctively expressed by Dclk1+ tuft-like tumor cells in mouse intestinal tumors. Using this tuft cell marker, we compared and analyzed the transcriptome of Lgr5-tuft marker-, Lgr5+tuft marker-, Lgr5-tuft marker+, and Lgr5+tuft marker+ tumor cells. These analyses revealed that tuft-like tumor cells in the intestinal tumors comprise two distinct subsets: highly differentiated tuft-like tumor cells (Lgr5-tuft marker+ cells) and tuft-like tumor cells with TCS potential (Lgr5+tuft marker+ cells).

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Lgr5+ve stem cells in nephrogenesis

Project description:Multipotent stem cells and their lineage-restricted progeny drive nephron formation within the developing kidney. Validated markers of these early stem/progenitor populations are essential for deciphering their in vivo function and for evaluating their clinical potential for treating adult kidney disease. Here, we document expression of the adult stem cell marker Lgr5 in the developing kidney and assess the stem/progenitor identity of Lgr5+ve cells via in vivo lineage tracing. The appearance and localization of Lgr5+ve cells coincided with that of the S-shaped body around E14. Lgr5 expression remained restricted to cell clusters within developing nephrons in the cortex until P7, when expression was permanently silenced. In vivo lineage tracing identified Lgr5 as a marker of a novel progenitor population within nascent nephrons dedicated to generating the thick ascending limb of Henle's loop and distal convoluted tubule. The Lgr5 surface marker and experimental models described here will be invaluable for deciphering the contribution of early nephron stem cells to developmental defects and for isolating human nephron progenitors as a prerequisite to evaluating their therapeutic potential. Metanephric kidneys of timed pregnancies of ~14 days of gestation were harvested and cultured for ~10 days. Lgr5-EGFP-Ires-CreERT2-positive embryonic kidneys were identified by fluorescence microscopy and enzymatically digested to a single cell solution. GFPhi and GFPneg cells were sorted by flow cytometry (MoFlo; Dako). RNA, isolated using RNeasy (Qiagen), was analyzed using the Affymetrix platform.

2012-09-04 | E-GEOD-39881 | biostudies-arrayexpress

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