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Expression data from Ad-β-catenin-GFP or Ad-GFP infected cardiomyocytes

ABSTRACT: The Wnt pathway is a key regulator of embryonic development, cell growth, differentiation, polarity formation, neural development, carcinogenesis, and stem cell self-renewal, and deregulation of the Wnt signalling is associated with many human disease. The central player in the Wnt pathway is β-catenin, A recent study has shown that β-catenin/Tcf/Lef signaling pathway is an essential growth-regulatory pathway in cardiomyocytes. We used DNA microarrays to detail the global trends in gene expression underlying β-catenin-overexpressed cardiomyocytes and identified distinct classes of up- or down-regulated genes during this process. Our findings suggest that β-catenin plays a critical role in regulating cardiac dysfunction at transcriptional level and may provide novel insight into how β-catenin modulates heart diseases.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE34772 | GEO | 2011/12/30

SECONDARY ACCESSION(S): PRJNA150345

REPOSITORIES: GEO

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Expression data from Ad-β-catenin-GFP or Ad-GFP infected cardiomyocytes

Project description:The Wnt pathway is a key regulator of embryonic development, cell growth, differentiation, polarity formation, neural development, carcinogenesis, and stem cell self-renewal, and deregulation of the Wnt signalling is associated with many human disease. The central player in the Wnt pathway is β-catenin, A recent study has shown that β-catenin/Tcf/Lef signaling pathway is an essential growth-regulatory pathway in cardiomyocytes. We used DNA microarrays to detail the global trends in gene expression underlying β-catenin-overexpressed cardiomyocytes and identified distinct classes of up- or down-regulated genes during this process. Our findings suggest that β-catenin plays a critical role in regulating cardiac dysfunction at transcriptional level and may provide novel insight into how β-catenin modulates heart diseases. Cardiomyocytes were infected with GFP control or β-catenin adenoviruses for RNA extraction and hybridization on Affymetrix microarrays. We sought to define the effects of β-catenin on the global programme of gene expression in primary cardiomyocytes. To that end, neonatal rat cardiomyocytes were infected with GFP control (G) or β-catenin adenovirus (B) for 24 hours.

2011-12-30 | E-GEOD-34772 | biostudies-arrayexpress

TCF/LEF dependent and independent regulation of Wnt/beta-catenin transcription

Project description:During canonical Wnt signalling the activity of nuclear beta-catenin is largely mediated by the TCF/LEF family of transcription factors. To challenge this view we used the CRISPR/Cas9 genome editing approach to generate HEK 293T cell clones simultaneously carrying loss-of-function alleles of all four TCF/LEF genes. Exploiting unbiased whole transcriptome sequencing studies, we found that a subset of beta-catenin transcriptional targets did not require TCF/LEF factors for their regulation. Consistent with this finding, we observed in a genome-wide analysis that beta-catenin occupied specific genomic regions in the absence of TCF/LEF. Finally, we revealed the existence of a transcriptional activity of beta-catenin that specifically appears when TCF/LEF factors are absent, and refer to this as beta-catenin-GHOST response. Collectively, this study uncovers a previously neglected modus operandi of beta-catenin that bypasses the TCF/LEF transcription factors.

2018-11-22 | E-MTAB-7028 | biostudies-arrayexpress

TCF/LEF dependent and independent regulation of Wnt/beta-catenin transcription

2018-11-02 | E-MTAB-7029 | biostudies-arrayexpress

The oncogenic transcription factor FOXQ1 is a bimodal regulator of Wnt target genes

Project description:The forkhead box transcription factor FOXQ1 is aberrantly induced in various cancers, and contributes to tumour growth and metastasis. It has been suggested that the oncogenic potential of FOXQ1 may be explained by its activation of the Wnt/β-catenin signalling pathway. However, the mode of action of FOXQ1 in the Wnt pathway remains to be resolved. Here we report that FOXQ1 is bimodal transcriptional regulator of Wnt target gene expression in normal and cancer cells. Using co-immunoprecipitation, proximity proteomics, and reporter assays, we show that FOXQ1 partly engages the Wnt transcriptional complex to promote gene expression via TCF/LEF transcription factors.

2022-10-05 | PXD035624 | Pride

Cell-line-specific gene expression changes following inactivation of the CTNNB1 gene in human colorectal cancer cell lines

Project description:Unrestrained transcriptional activity of β-CATENIN and its binding partner TCF7L2 frequently underlies colorectal tumor initiation and is considered an obligatory oncogenic driver throughout intestinal carcinogenesis. Yet, the TCF7L2 gene carries inactivating mutations in about 10 % of colorectal tumors and is non-essential in colorectal cancer (CRC) cell lines. To determine whether CRC cells acquire TCF7L2-independence through cancer-specific compensation by other T-cell factor (TCF)/lymphoid enhancer‑binding factor (LEF) family members, or rather lose addiction to β-CATENIN/TCF7L2-driven gene expression altogether, we generated multiple CRC cell lines entirely negative for TCF/LEF or β-CATENIN expression. Viability of these cells demonstrates complete β‑CATENIN- and TCF/LEF-independence, albeit one β-CATENIN-deficient cell line eventually became senescent. Absence of TCF/LEF proteins and β-CATENIN consistently impaired CRC cell proliferation, reminiscent of mitogenic effects of WNT/β-CATENIN signaling in the healthy intestine. Despite this common phenotype, β-CATENIN-deficient cells exhibited highly cell-line-specific gene expression changes with little overlap between β-CATENIN- and TCF7L2-dependent transcriptomes. Apparently, β‑CATENIN and TCF7L2 control sizeable fractions of their target genes independently from each other. The observed divergence of β-CATENIN and TCF7L2 transcriptional programs, and the finding that neither β-CATENIN nor TCF/LEF activity is strictly required for CRC cell survival has important implications when evaluating these factors as potential drug targets.

2022-12-13 | GSE199835 | GEO

The oncogene FOXQ1 is a selective activator of Wnt/β-catenin signalling

Project description:The forkhead box transcription factor FOXQ1 is aberrantly induced in various cancers, and contributes to tumour growth and metastasis. It has been suggested that the oncogenic potential of FOXQ1 may be explained by its activation of the Wnt/β-catenin signalling pathway.However, the mode of action of FOXQ1 in the Wnt pathway remains to be resolved. Here we report that FOXQ1 is bimodal transcriptional activator of Wnt target gene expression in normal and cancer cells. Using co-immunoprecipitation, proximity proteomics, and reporter assays, we show that FOXQ1 engages the Wnt transcriptional complex to promote gene expressionvia TCF/LEF transcription factors.

2022-10-05 | PXD030464 | Pride

Gene Expression Analysis of WT and dnTCF4-expressing Short-Term Hematopoietic Stem Cells (ST-HSC)

Project description:The canonical Wnt signaling pathway is mediated by interaction of b-catenin with the TCF/LEF transcription factors and subsequent transcriptional activation of Wnt-target genes. In the hematopoietic system, the function of the pathway has been mainly investigated by genetic manipulation of b-catenin. However, this approach does not allow to discriminate between TCF/LEF dependent or independent b-catenin activity. Here, we employed a transgenic mouse model expressing a truncated dominant negative form of the human TCF4 transcription factor (dnTCF4) which abrogates activation of Wnt target genes even when b-catenin is stabilized and translocated into the nucleus while preserving its TCF/LEF independent activities. The disruption of the b-catenin-TCF/LEF interaction results in reduced granulocytic differentiation accompanied with an accumulation of short-term hematopoietic stem cells (ST-HSC) and granulocytic progenitors. In order to investigate the mechanism responsible for the insufficient production of granulocytes, we performed a transcriptomic analysis of ST-HSC from dnTCF4-expressing and control WT mice.

2020-08-25 | GSE139668 | GEO

Identification of beta-catenin binding regions in SW480 cells

Project description:Deregulation of canonical Wnt/beta-catenin pathway is one of the earliest events in the pathogenesis of colon cancer. Mutations in APC or CTNNB1 (beta-catenin gene) are highly frequent in colon cancer and cause aberrant stabilization of b-catenin, which activates the transcription of Wnt target genes by binding to chromatin via the TCF/LEF transcription factors. Here we report an integrative analysis of genome-wide chromatin occupancy of b-catenin by chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) and gene expression profiling by microarray analysis upon RNAi-mediated knockdown of beta-catenin in colon cancer cells (GSE53656). Immunoprecipitated samples from human colon cancer SW480 cells with antibodies against beta-catenin and control IgG respectively were used for ChIP-seq experiments.

2014-03-12 | E-GEOD-53927 | biostudies-arrayexpress

The fusion protein SS18-SSX1 employs core Wnt pathway transcription factors to induce a partial Wnt signature in synovial sarcoma

Project description:Expression of the SS18/SYT-SSX fusion protein is believed to underlie the pathogenesis of synovial sarcoma (SS). Recent evidence suggests that deregulation of the Wnt pathway may play an important role in SS but the mechanisms whereby SS18-SSX might affect Wnt signaling remain to be elucidated. Here, we show that SS18/SSX tightly regulates the elevated expression of the key Wnt target AXIN2 in primary SS. SS18-SSX is shown to interact with TCF/LEF, TLE and HDAC but not β -catenin in vivo and to induce Wnt target gene expression by forming a complex containing promoter-bound TCF/LEF and HDAC but lacking β -catenin. Our observations provide a tumor-specific mechanistic basis for Wnt target gene induction in SS that can occur in the absence of Wnt ligand stimulation.

2016-02-23 | GSE78159 | GEO

ChIP-chip from mouse keratinocytes with Plakoglobin and β-catenin

Project description:Plakoglobin (PG; γ-Catenin, JUP) is a protein with controversial function. First described as a component of intercellular junctions, it has remained unresolved whether this near-ubiquitously expressed protein acts as a genuine transcriptional regulator in adult tissue like its closest relative β-catenin. Here we have mapped the global gene targets of PG by ChIP-chip in differentiating skin keratinocytes. Applying a peak algorithm, over 5’000 high-confidence PG target promoters were identified and 2’000 for β-catenin with an overlap of 38%. Bioinformatics analyses most significantly associated PG target genes with the Wnt signaling pathway as well as relevant pathways for keratinocyte differentiation. Using a combination of wild-type, PG, β-catenin and PG/β-catenin double null keratinocytes, PG was functionally validated as a LEF/TCF-dependent transcriptional regulator. These data challenge the current understanding of Wnt signaling, one of the most important pathways in tissue homeostasis, by identifying PG as a potent LEF/TCF-dependent transcriptional regulator which functionally overlaps with β-catenin.

2017-12-01 | GSE37343 | GEO

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