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Subpopulations of activated hepatic stellate cells defined and inhibited by WT1 expression

ABSTRACT: Subpopulations of activated hepatic stellate cells defined and inhibited by WT1 expression

PROVIDER: PRJNA400188 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5976580.fastq.gz	Fastqsanger.gz
	SRR5976571.fastq.gz	Fastqsanger.gz
	SRR5976581.fastq.gz	Fastqsanger.gz
	SRR5976572.fastq.gz	Fastqsanger.gz
	SRR5976582.fastq.gz	Fastqsanger.gz

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Discrete WT1-positive hepatic fibrogenic cell lineages of distinct developmental mesothelial origin are paradoxically inhibited by WT1

Project description:Activated hepatic stellate cells orchestrate scar formation during fibrotic liver injury. Recent evidence has shown limited quiescent precursor derivation from the mesoderm during development. Here, we use lineage-tracing from development, through adult homeostasis, to adult fibrotic injury, to show that discreet subpopulations of activated hepatic stellate cells are defined by expression of WT1, a transcription factor controlling morphological transitions in organogenesis and adult homeostasis. Morphologically and transcriptionally distinct subpopulations are evident in fibrotic human disease and animal models. Populations defined by WT1 expression after injury derive from a discreet population of quiescent adult precursors originating from the embryonic mesothelium. WT1-deletion permits morphological transition to an enhanced fibrotic myofibroblast phenotype. Our findings demonstrate functional heterogeneity of adult scar-forming cells that can be whole-life traced back through specific quiescent precursors in adult homeostasis to differential origin in development, and defines WT1 as a paradoxical anti-fibrotic regulator during adult injury.

2019-08-21 | GSE103103 | GEO

Whole genome expression analysis of subpopulations of activated hepatic stellate cells defined by WT1 expression

Project description:Transciptional heterogeneity of scar-orchestrating cells in liver fibrosis, defined by WT1 expression, after chronic tetrachloride injury in vivo (WT1-high and WT1-low) or activation in vitro (WT1-negative).

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Subpopulations of activated hepatic stellate cells defined and inhibited by WT1 expression

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

2019-08-21 | GSE103108 | GEO

Opposing Roles of Hepatic Stellate Cell Subpopulations in Hepatocarcinogenesis

Project description:Opposing Roles of Hepatic Stellate Cell Subpopulations in Hepatocarcinogenesis

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Project description:Whole genome expression analysis of subpopulations of activated hepatic stellate cells defined by WT1 expression

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Opposing Roles of Hepatic Stellate Cell Subpopulations in Hepatocarcinogenesis

Project description:Hepatocellular carcinoma (HCC), the fourth leading cause of cancer mortality, develops almost exclusively in patients with chronic liver disease (CLD) and advanced fibrosis. Here we interrogated functions of hepatic stellate cells (HSC), the main source of liver fibroblasts, during hepatocarcinogenPesis. Genetic depletion, activation or inhibition established HSC as tumour-promoting in mouse models of HCC. HSC were enriched in the preneoplastic environment, where they closely interacted with hepatocytes and modulated hepatocarcinogenesis by regulating hepatocyte proliferation and death. Analysis of mouse and human HSC subpopulations and their associated mediators by single cell RNA-sequencing in conjunction with genetic ablation revealed dual functions of HSC in hepatocarcinogenesis. Hepatocyte growth factor, enriched in quiescent and cytokine-producing HSC (cyHSC), protected from hepatocyte death and HCC development. In contrast, type I collagen, enriched in activated myofibroblastic HSC (myHSC), promoted proliferation and tumour development via increased stiffness and TAZ activation in pretumoural hepatocytes and via activation of discoidin domain receptor 1 in established tumours. An increasing HSC dysbalance between cyHSC and myHSC during liver disease progression was associated with elevated HCC risk in patients. In summary, the dynamic shift of HSC subpopulations and their mediators during CLD is associated with a switch from HCC protection to HCC promotion. This SuperSeries is composed of the SubSeries listed below.

2022-08-26 | GSE212047 | GEO

Desmoplastic small round cell tumor is dependent on EWS-WT1

Project description:Desmoplastic small round cell tumor (DSRCT) is a rare and aggressive soft tissue malignancy. The disease is defined by the oncogenic EWS-WT1 transcription factor. However, the dependence of the tumor on this target has not been well-established and no EWS-WT1 targeted therapy has translated to the clinic. In this report we establish the dependence of DSRCT on EWS-WT1 as well as define a gene signature and a comprehensive list of downstream targets. The selective silencing of EWS-WT1 leads to the marked suppression of proliferation of both JN-DSRCT1 and BER cells. Loss of the fusion protein results in morphologic changes in the cells and eventual cellular apoptosis. RNA sequencing demonstrates large scale gene expression changes attributable to EWS-WT1 with several hundred induced or repressed downstream targets of the fusion. We conclude DSRCT is dependent on the EWS-WT1 transcription factor for cell survival. The presence of EWS-WT1 leads to enrichment of genes involved in aberrant cell differentiation and development as well as those involved in tumor metastasis.

2020-05-04 | GSE137561 | GEO

WT1 Trio Peptide-vaccine for Rare Cancers

Project description:Interventions: A patient is vaccinated with Montanide ISA51-adjuvanted WT1 Trio cancer vaccine consisting of two WT1 CTL peptides (WT1-126 and WT1-235) and one WT1 HTL peptide (WT1-332) (2mg each) seven times at the interval of two weeks. Primary outcome(s): Induction of WT1-specific immune responses assessed by WT1-related tests such as WT1-DTH skin reaction and serum levels of WT1 peptide IgG autoantibody at 1M, 2M, and 3M of WT1 Trio vaccine. Study Design: Single arm Non-randomized

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Project description:Interventions: A patient is vaccinated with Montanide ISA51-adjuvanted WT1 Trio cancer vaccine consisting of two WT1 CTL peptides (WT1-126 and WT1-235) and one WT1 HTL peptide (WT1-332) (2mg each) seven times at the interval of two to four weeks. The interval can be changed within a range from one to 16 weeks. Primary outcome(s): Induction of WT1-specific immune responses assessed by WT1-related tests such as WT1-DTH skin reaction, serum levels of WT1 peptide IgG autoantibody, and frequency of WT1-CTL in PB * This is evaluated at the interval ranging from 6 to 12 months. Study Design: Single arm Non-randomized

| 2638831 | ecrin-mdr-crc

MEF-mKras-WT1

Project description:K-ras is one of the most frequently mutated human oncogenes. Activation of K-ras can lead to either senescence or proliferation in primary cells. The precise mechanism governing these distinct outcomes remains unclear. Here we utilized a loss-of-function screen to assess the role of specific genes identified as potential key regulators of K-ras driven oncogenesis. Using this approach, we identify the transcription factor Wt1 as an inhibitor of senescence in primary cells expressing oncogenic K-ras. Deletion or suppression of Wt1 expression leads to senescence of primary cells expressing oncogenic K-ras under the control of the native promotor at physiological levels, but has no effect on cells expressing wild-type K-ras. Wt1 contributes to K-ras driven lung tumorigenesis in vivo and loss of Wt1 is specifically deleterious to human lung cancer cell lines that are dependent on oncogenic K-ras. Taken together, these observations reveal a novel role for Wt1 as a key regulator of the complex genetic network required for the oncogenic effect of the small GTPase K-ras. We compare the expression profiles of Wild type, K-ras mutant, Wt1-null, and double K-ras mutant/Wt1-null mouse embryonic fibroblasts (MEFs). The study provides insights into the transcriptional role of Wt1 in the context of oncogenic K-ras.

2010-03-01 | GSE15325 | GEO

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