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Leukemia associated mutant Wilms' tumour gene 1 protein promotes expansion of human hematopoietic progenitor cells

ABSTRACT: Analysis of gene expression levels in hematopoietic progenitor cells retrovirally transduced with full-length WT1(+/-) or a WT1-mutant lacking zinc-finger, WT1(delZ) cultured in vitro for 14 days. The hypothesis tested in this study was that the WT1-mutant confers an increased proliferation rate after 14 days in culture and an erythroid phenotype. Results provide information of upregulation of some genes associated with cellcycle progression, upregulated genes connected with erythropoiesis and downmodulation of some genes associated with myeloid differentiation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE47560 | GEO | 2013/06/21

SECONDARY ACCESSION(S): PRJNA206072

REPOSITORIES: GEO

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Leukemia associated mutant Wilms' tumour gene 1 protein promotes expansion of human hematopoietic progenitor cells

Project description:Analysis of gene expression levels in hematopoietic progenitor cells retrovirally transduced with full-length WT1(+/-) or a WT1-mutant lacking zinc-finger, WT1(delZ) cultured in vitro for 14 days. The hypothesis tested in this study was that the WT1-mutant confers an increased proliferation rate after 14 days in culture and an erythroid phenotype. Results provide information of upregulation of some genes associated with cellcycle progression, upregulated genes connected with erythropoiesis and downmodulation of some genes associated with myeloid differentiation. Total RNA obtained from CD34+ progenitor cells in suspension cultures for 14 days.

2013-06-21 | E-GEOD-47560 | biostudies-arrayexpress

MicroRNA profiling of Wilms Tumour 1 deleted and induced embryonic stem cells

Project description:We report the microRNA profiles of the mouse embryonic stem cell (E14IV), which have been deleted for tumour suppressor Wilms' Tumour 1 (WT1), and induced with retinoic acid. Additionally, cells that had an inducibe WT1 expression where also used to compare the microRNA profile during different time points of WT1 induction.

2024-03-26 | GSE169684 | GEO

CTNNB1 mutations and overexpression of Wnt/beta-catenin target genes in WT1-mutant Wilms' tumors

Project description:Gain-of-function mutations in exon 3 of beta-catenin (CTNNB1) are specific for Wilms' tumors that have lost WT1, but 50% of WT1-mutant cases lack such "hot spot" mutations. To ask whether stabilization of beta-catenin might be essential after WT1 loss, and to identify downstream target genes, we compared expression profiles in WT1-mutant versus WT1 wild-type Wilms' tumors. Supervised and nonsupervised hierarchical clustering of the expression data separated these two classes of Wilms' tumor. The WT1-mutant tumors overexpressed genes encoding myogenic and other transcription factors (MOX2, LBX1, SIM2), signaling molecules (TGFB2, FST, BMP2A), extracellular Wnt inhibitors (WIF1, SFRP4), and known beta-catenin/TCF targets (FST, CSPG2, CMYC). Beta-Catenin/TCF target genes were overexpressed in the WT1-mutant tumors even in the absence of CTNNB1 exon 3 mutations, and complete sequencing revealed gain-of-function mutations elsewhere in the CTNNB1 gene in some of these tumors, increasing the overall mutation frequency to 75%. Lastly, we identified and validated a novel direct beta-catenin target gene, GAD1, among the WT1-mutant signature genes. These data highlight two molecular classes of Wilms' tumor, and indicate strong selection for stabilization of beta-catenin in the WT1-mutant class. Beta-Catenin stabilization can initiate tumorigenesis in other systems, and this mechanism is likely critical in tumor formation after loss of WT1. Keywords: single channel

2006-10-28 | GSE6120 | GEO

Transcription profiling of human WT1-mutant versus WT1 wild-type Wilms tumors

2008-06-14 | E-GEOD-6120 | biostudies-arrayexpress

Chemotherapy and terminal skeletal muscle differentiation in WT1 mutant Wilms tumors

Project description:Gene expression profiling of six chemotherapy and two untreated WT1 mutant tumors; see also GSE63616

2018-06-17 | GSE102723 | GEO

Classification of a frameshift/extended and a stop mutation in WT1 as gain of function mutations which activate cell cycle genes and promote Wilms tumor cell proliferation

Project description:The Wilms tumor 1 (WT1) gene encodes a zinc finger transcription factor important for normal kidney development. WT1 is a suppressor for Wilms tumor development and an oncogene for diverse malignant tumors. We recently established cell lines from primary Wilms tumors and identified the corresponding WT1 mutations (see GSE18058). To investigate the function of mutant WT1 proteins we performed WT1 knockdown experiments in primary Wilms tumor cell lines with a frameshift/extension (p.V432fsX87 = Wilms3) and a stop mutation (p.P362X = Wilms2) of WT1, followed by genome wide gene expression analysis. A detailed analysis of these gene expression data using MetaCore enabled us to classify the WT1 mutations as gain of function mutations. The mutant WT1Wilms2 and WT1Wilms3 proteins acquired an ability to modulate the expression of a highly significant number of genes from the G2/M phase of the cell cycle, and WT1 knockdown experiments showed that they are required for Wilms tumor cell proliferation. Data from the literature show that p53 negatively regulates the activity of a large number of these genes which are also part of a core proliferation cluster in diverse human cancers. Our data strongly suggest that mutant WT1 proteins facilitate expression of these cell cycle genes by antagonizing transcriptional repression mediated by p53. In light of this it is important to note that mutant WT1 has an ability to physically interact with the tumor suppressor p53. Together the findings show for the first time, that mutant WT1 proteins have a gain of function and act as oncogenes for Wilms tumor development by regulating Wilms tumor cell proliferation. siWT1 mediated knockdown in two Wilms tumor cell lines one and two days after transfection versus non-silencing controls

2014-05-12 | E-GEOD-54635 | biostudies-arrayexpress

Classification of a frameshift/extended and a stop mutation in WT1 as gain of function mutations which activate cell cycle genes and promote Wilms tumor cell proliferation

2014-05-12 | GSE54635 | GEO

The Wilms' tumour 1 transcription factor regulates epigenetic states via DNA methyltransferase 3A

Project description:The Wilms' tumour 1 transcription factor regulates epigenetic states via DNA methyltransferase 3A. The data consists of two Nimblegen promoter/CpG island microarrays hybridized with MCIP DNA immunoprecipitated from either a HEK293-derived cell line expressing a heterologous WT1 cDNA (W210) or a control cell line containing the expression vector (IP100), both hybridized against input DNA.

2012-11-05 | E-GEOD-39713 | biostudies-arrayexpress

Homeobox regulator Wilms tumour 1 (WT1) is displaced by androgen receptor at cis-regulatory sites in the endometrium of PCOS patients.

Project description:Polycystic ovary syndrome (PCOS) is a common gynaecological disorder, characterised by elevated circulating androgens and increased expression of androgen receptor (AR) and by downregulation of Wilms Tumour 1 in the endometrium, The objectives of this study are: 1) Understand the functional role of WT1 in regulating decidualization response in healthy endometrial tissue, and 2) understand how interactions between aberrant WT1 and AR expression in PCOS patients result in dysregulation of deciduallization processes

2024-02-16 | GSE240055 | GEO

Gene expression studies of WT1 mutant Wilms tumor cell lines in the frame work of published kidney development data reveals their early kidney stem cell origin

Project description:In order to get a better insight into the timing of WT1 mutant Wilms tumor development, we compared the gene expression profiles of nine established WT1 mutant Wilms tumor cell lines with published data from different kidney cell types during development. Publications describing genes expressed in nephrogenic precursor cells, ureteric bud cells, more mature nephrogenic epithelial cells and interstitial cell types were used. These studies uncovered that the WT1 mutant Wilms tumor cells lines express genes from the earliest nephrogenic progenitor cells, as well as from more differentiated nephron cells with the highest expression from the stromal/interstitial compartment. The expression of genes from all cell compartments points to an early developmental origin of the tumor in a common stem cell. Although variability of the expression of specific genes was evident between the cell lines the overall expression pattern was very similar. This is likely dependent on their different genetic backgrounds with distinct WT1 mutations and the absence/presence of mutant CTNNB1.

2023-02-08 | GSE220082 | GEO

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