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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE240055 | GEO | 2024/02/16

REPOSITORIES: GEO

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Genome-wide map of AR-targets in human endometrial stromal cells treated with DHT.

Project description:Polycystic ovary syndrome (PCOS) is a common gynaecological disorder, characterised by elevated circulating androgens and aberrant expression of androgen receptor (AR) in the endometrium: The objective of this study is to evaluate the targets of AR in PCOS patients. Overexpression of AR and altered endometrial signalling pathways in PCOS patients may impact on a correct decidualization response, critically affecting the events surrounding embryo implantation and causing infertility.

2019-12-31 | GSE119432 | GEO

Expression data from non-decidualized and decidualized endometrial stromal cell (ESCs) with or without WT1 knockdown

Project description:Wilms tumor 1 (WT1) regulates the expression of insulin-like growth factor-binding protein-1 (IGFBP-1) and prolactin (PRL) during decidualization of human endometrial stromal cells (ESCs). However, other roles of WT1 in decidualization have not been fully clarified. We used microarrays to identify the physiological roles of WT1 in the regulation of cellular functions of human ESCs during decidualization.

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Transcription profiling of human WT1-mutant versus WT1 wild-type 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. Experiment Overall Design: Identification of WNT/Beta-Catenin or WT1 target genes. 39 individual samples.

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

Wilms' tumor 1 WT1(-KTS) isoform time course induction in U2OS cells

2007-06-21 | GSE5117 | GEO

Oviductal fluid LC-MS/MS - The Wilms tumor protein Wt1 contributes to female fertility by regulating oviductal proteostasis

Project description:After fertilization the developing mammalian embryo migrates through the oviduct before it implants in the uterus. In order to prevent tubal pregnancy or failed implantation, development and migration of the embryo has to be tightly coordinated1. The precise molecular basis for the regulation of this maternal-embryonic interaction is largely unknown. Here we show that the Wilms tumor suppressor protein Wt1 is a critical regulator of the interaction between the maternal environment and the early embryo. Our results indicate that subfertility in Wt1ko/+ females is a maternal effect caused by the Wt1-dependent de-regulation of Prss29, encoding a serine protease. Notably, blocking Prss29 activity was sufficient to rescue subfertility in Wt1ko/+ female mice indicating Prss29 as a critical factor in female fertility. Furthermore, we have identified a missense mutation in a patient with idiopathic infertility leading to an amino acid exchange within the zinc finger domain of WT1 and resulting in reduced DNA binding. We demonstrate that Wt1 represses expression of Prss29 and that its de-repression and precocious expression in the oviduct interferes with pre-implantation development. Our study reveals a novel role for Wt1 in early mammalian development and identifies proteases as critical mediators of the maternal-embryonic crosstalk. We believe that our data regarding the importance of a proteostatic environment in the oviduct are also relevant for female fertility in humans. We anticipate that our findings will form the basis for the identification of further causes of idiopathic infertility.

2017-04-04 | PXD003283 | Pride

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

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

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miRNAs expression profile of the cumulus cell samples with PCOS and non-PCOS

Project description:To reveal microRNAs expression differences in cumulus cells between polycystic ovary syndrome (PCOS) and non-PCOS women. miRNAs expression profile of the cumulus cell samples with PCOS and non-PCOS were determined by Affymetrix miRNA 2.0. Six pooled RNAs from CC samples (three PCOS and three non-PCOS pooled RNAs) were separately analyzed on 6 GeneChip miRNA 2.0 Array (miRBase V15)

2015-04-28 | E-GEOD-68285 | biostudies-arrayexpress

Transcription profiling of human Wilms tumor 1 WT1(-KTS) isoform time series induction in U2OS cells

Project description:The Wilms' tumor suppressor gene (WT1) encodes a zinc finger transcription factor that plays important roles during development of several organs including metanephric kidneys. A number of WT1 target genes have been identified, but the detailed mechanisms by which WT1 orchestrates renal development remain elusive. To identify WT1 target genes relevant to development, genome-wide expression profiling was performed using oligonucleotide microarrays representing 39,000 human transcripts Experiment Overall Design: Sample_source_name: UB27 cells, U2OS cells with Tetracycline-repressible WT1(-KTS) expression Experiment Overall Design: Sample_characteristics: U2OS cell line (osteosarcoma; female), Tetracycline-repressible WT1(-KTS) expression, time-course induction Experiment Overall Design: of WT1(-KTS) expression Experiment Overall Design: Sample_description: WT1(-KTS) expression was induced for 4, 8 or 12 Experiment Overall Design: hrs and the expression profile of each time-points was compared to the Experiment Overall Design: uninduced sample (0 hr).

2008-06-13 | E-GEOD-5117 | biostudies-arrayexpress

miRNAs expression profile of the cumulus cell samples with PCOS and non-PCOS

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