Quiescence specific β-catenin transcriptional networks in myogenic cells
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ABSTRACT:
PROVIDER: PRJNA593721 | ENA |
REPOSITORIES: ENA
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Project description:Wnt/β-catenin signaling is active during cellular quiescence in muscle myoblasts. Exposure of quiescent myoblasts to Wnt3a led to deregulation of genes associated with both myogenic differentiation and proliferation. Genome-wide analysis Ctnnb1 by ChIP-chip revealed quiescence-specific enrichment on genes of multiple functional classes. The major class of genes bound by Ctnnb1were Wnt pathway genes and all occupied promoters were highly enriched for TCF DNA binding motifs. Cross-comparison of ChIP-Chip with transcriptome data revealed both transcriptional activation as well as repression in Ctnnb1 occupied genes. Inhibition of Ctnnb1-mediated transactivation using shRNA and pharmacological agents led to de-regulation of the quiescence-associated transcriptional profile. Ctnnb1 binding is associated with repression of myogenic genes and cell cycle progression factors while maintaining differential response by these genes to Wnt signaling during quiescence. Microarray analysis of Wnt3A treated G0 myoblasts compared to untreated G0 cells
2020-03-31 | GSE141506 | GEO
Project description:We used interaction and expression proteomic techniques in conjunction with RNA-Seq transcriptomic analysis to analyse how a β-catenin stabilizing mutation alters molecular networks in colorectal cancer cells. Integrated computational analyses of allowed us to identify significantly altered sub-networks linked to β-catenin oncogenesis.
2018-05-18 | PXD006053 | Pride
Project description:e used interaction and expression proteomic techniques in conjunction with RNA-Seq transcriptomic analysis to analyse how a β-catenin stabilizing mutation alters molecular networks in colorectal cancer cells. Integrated computational analyses of allowed us to identify significantly altered sub-networks linked to β-catenin oncogenesis.
2018-10-05 | PXD006051 | Pride
Project description:The inability of the adult mammalian heart to regenerate represents a fundamental barrier in heart failure management. In contrast, the neonatal heart retains a transient regenerative capacity, but the underlying mechanisms are not fully understood. Wnt/β-catenin signaling has been suggested as a key cardio-regenerative pathway. Here, we show that Wnt/β-catenin signaling potentiates neonatal mouse cardiomyocyte proliferation in vivo and immature human pluripotent stem cell-derived cardiomyocyte (hPSC-CM) proliferation in vitro. In contrast, Wnt/β-catenin signaling in adult mice is cardioprotective but fails to induce cardiomyocyte proliferation. Transcriptional profiling of neonatal mouse and hPSC-CM revealed a core Wnt/β-catenin-dependent transcriptional network governing cardiomyocyte proliferation. In contrast, β-catenin failed to re-engage this proliferative gene network in the adult heart, which instead reverted to a neonatal-like glycolytic program. These findings suggest that Wnt/β-catenin drives distinct transcriptional networks in regenerative and non-regenerative cardiomyocytes, which may contribute towards the inability of the adult heart to regenerate following injury.
2020-11-04 | GSE150521 | GEO
Project description:Although tsRNA was reported to have the ability to modulate a variety of physiological processes analogous to miRNA, the possible regulatory functions and mechanisms of tsRNAs related to the pharmacological effects of small molecules are still obscure. Herein it is shown that the natural product eurycomalactone (ELT) can reversibly switch hepatocellular carcinoma (HCC) PLC/PEF/5 and HUH7 cells into a quiescence state characterized by cell proliferation inhibition without cell death, cell cycle arrest at G0/G1 phase and cell reactivation after drug withdrawal. On the basis that β-catenin activity might mediate the proliferation or quiescence of cancer cells, the total, cytoplasmic and nuclear β-catenin, as well as its target proteins, c-myc, CD44 and cyclin D1, are all shown to be significantly weakened by ELT. Subsequently, two new tsRNAs, namely 5'tRFAla and 5'tiRNAAla, which match well with the mRNAs of Dishevelled proteins DVL2 and DVL3, two vital upstream regulators of β-catenin, are found to be decreased significantly in ELT-treated PLC/PEF/5 cells. The concentrations of the DVL2 and DVL3 proteins are similarly reduced. Accordingly, it is suggested that ELT decreases 5'tRFAla and 5'tiRNAAla levels and so suppressing the translation of their matched DVL2 and DVL3 mRNAs that thereby inhibits the β-catenin pathway and so reversibly switching HCC cells into a quiescence state. As such, this study suggests that, like miRNAs, tsRNAs might activate the translation of their matched mRNAs in non-dividing cells and so providing a possible means for suppressing tumor cell growth
2023-07-10 | GSE236560 | GEO
Project description:Interventions: Case series:Nil
Primary outcome(s): Ecadherin, beta catenin, CDX - 2, SOX - 2
Study Design: Non randomized control
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Project description:To identify evolutionarily conserved Beta-catenin protein interactions, Beta-catenin mRNA from various metazoans was injected into Xenopus embryos and immunopurified at gastrula stage. Beta-catenin complexes were then separated on an SDS-PAGE gel and subjected mass spectrometric analysis
2023-07-08 | PXD035167 | JPOST Repository
Project description:To validate the suitability of two commonly used colorectal cancer cell lines, DLD1 and SW480, as model systems to study colorectal carcinogenesis, we treated these cell lines with beta-catenin siRNA and identified beta-catenin target genes using DNA microarrays. The list of identified target genes was compared to previously published beta-catenin target genes found in the PubMed and the GEO databases. Based on the large number of beta-catenin target genes found to be similarly regulated in DLD1, SW480 and LS174T as well as the large overlap with confirmed β-catenin target genes, we conclude that DLD1 and SW480 colon carcinoma cell lines are suitable model systems to study beta-catenin regulated genes and signaling pathways 12 arrays (2 cell lines, 2 treatments, 3 biological replicates)
2013-12-31 | E-GEOD-44097 | biostudies-arrayexpress
Project description:This study describes the systematic transcriptomic and expression and interaction proteomic analysis of isogenic HCT116 colorectal cancer cells with either mutant CTNNB1/Beta-catenin allele disrupted or wild-type CTNNB1/Beta-catenin allele disrupted.
2018-07-17 | GSE95670 | GEO
Project description:In nucleated cells, β-catenin, the key downstream effector of this pathway, is a dual function protein, regulating the coordination of gene transcription and cell–cell adhesion. The specific role of β-catenin in the anucleate platelet however remains elusive. Here, we performed a label-free quantitative proteomic analysis of β-catenin immunoprecipitates from human platelets identifying 9 co-immunoprecipitating proteins. GO biological pathway analysis revealed a significant enrichment of specific functional terms including 'cell adhesion', 'cell junction organization' and ‘adherens junction organization'. Our bioinformatics data suggests that human platelet β-catenin may be involved in facilitating cell adhesion and cell junctions. We found three proteins co-immunoprecipitating with β-catenin under both resting and activated conditions, four proteins under resting condition only and two proteins under activated condition only.
2018-07-05 | PXD008130 | Pride