The influence of WWOX gene on cellular pathways in neuronal differentiation of human neural stem cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA520917 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8528330.fastq.gz | Fastqsanger.gz | |||
| SRR8528331.fastq.gz | Fastqsanger.gz | |||
| SRR8528332.fastq.gz | Fastqsanger.gz | |||
| SRR8528333.fastq.gz | Fastqsanger.gz |
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Project description:The aim of presented study was to investigate in detail how depletion of WWOX gene disturbs signaling pathways pivotal in neuronal differentiation and CNS organogenesis. We conducted a global transcriptome analysis using CAGE method.
2019-06-01 | GSE126075 | GEO
Project description:Neuronal Wwox overexpression using CRISPRa in Drosophila melanogaster also expressing human AB42 can rescue amyloid related phenotypes. To understand how this may occur we performed bulk transcriptomics on day 14 heads from the same genotypes: 1) Control gRNA + lacZ expression control, 2) Control gRNA + amyloid, 3) Wwox gRNA + LacZ control, 4) Wwox gRNA + amyloid.
2025-04-18 | E-MTAB-14949 | biostudies-arrayexpress
Project description:The WWOX gene is a tumor suppressor probably involved in variety of cellular processes including and is ferquently downregulated in variety of cancer types. However, its role in endometrial cancerogenesis is not well described. The aim of this study was to characterize how WWOX may be involved in endometrial cancerogenesis, how it influences the basic cancer cell features and modifies cell expression profile.Our observations suggest that in ECC1 endometrial cancer cell line increased expression of WWOX may be involved in the initiation of EMT, leading to changes in cell adhesion and motility but also indicate its suppressive role in the process of mesenchymal phenotype acquisition, resulting in reduction of aggressiveness cell features
2014-09-03 | GSE61041 | GEO
Project description:The brain is the most functionally organized structure of all organs. It manages behavior, perception and higher cognitive functions. The WWOX gene is non-classical tumor suppressor gene, which has been shown to have an impact on proliferation, apoptosis and migration processes. Moreover, genetic aberrations in WWOX induce severe neuropathological phenotypes in humans and rodents. The aim of the present study was to investigate in detail the impact of WWOX on human neural progenitor cell (hNPC) maintenance and how depletion of WWOX disturbs signaling pathways playing a pivotal role in neuronal differentiation and central nervous system (CNS) organogenesis. hNPC with a silenced WWOX gene exhibited lowered mitochondrial redox potential, enhanced adhesion to fibronectin and extracellular matrix protein mixture, downregulation of MMP2/9 expression and impaired 3D growth. Global transcriptome analysis using cap analysis of gene expression (CAGE) found that WWOX downregulation significantly changes the expression of multiple genes engaged in cytoskeleton organization, adhesion, cell signaling and chromatin remodeling. The massive changes in gene expression caused by WWOX silencing may strongly affect the differentiation and migration of neurons in organogenesis, brain injury, cancerogenesis or neurodifferentiation. WWOX gene appears to be an important regulator of neural tissue architecture and function.
| S-EPMC6730490 | biostudies-literature
Project description:The WWOX gene is a tumor suppressor probably involved in variety of cellular processes including and is ferquently downregulated in variety of cancer types. However, its role in endometrial cancerogenesis is not well described. The aim of this study was to characterize how WWOX may be involved in endometrial cancerogenesis, how it influences the basic cancer cell features and modifies cell expression profile.Our observations suggest that in ECC1 endometrial cancer cell line increased expression of WWOX may be involved in the initiation of EMT, leading to changes in cell adhesion and motility but also indicate its suppressive role in the process of mesenchymal phenotype acquisition, resulting in reduction of aggressiveness cell features Well differentiated ECC1 endometrial cancer cells were stably transfected with WWOX cDNA.ECC1 cells transfected with an empty vector served as a control. Total mRNA was isolated to look for gene-expression differences induced by the WWOX overexpression.
2014-09-03 | E-GEOD-61041 | biostudies-arrayexpress
Project description:WWOX gene loss-of-function (LoF) has been associated with neuropathologies resulting in developmental, epileptic, and ataxic phenotypes of varying severity based on the level of WWOX dysfunction. WWOX gene biallelic germline variant p.Pro47Thr (P47T) has been causally associated with a new form of autosomal recessive cerebellar ataxia with epilepsy and intellectual disability (SCAR12). This mutation affects the WW1 protein binding domain of WWOX, impairing its ability to interact with canonical proline-proline-X-tyrosine motifs in partner proteins. We generated a mutant knock-in mouse model of Wwox P47T that phenocopies SCAR12. WwoxP47T/P47T mice displayed epilepsy, profound social behavior and cognition deficits, and poor motor coordination. These deficits progressed with age, and mice became practically immobile, suggesting severe cerebellar dysfunction. WwoxP47T/P47T mice exhibited signs of progressive neuroinflammation with elevated astro-microgliosis that increased with age. The cerebellar cortex displayed significantly reduced molecular and granular layer thickness and a strikingly reduced number of Purkinje cells with degenerated dendrites. Transcriptome profiling from various brain regions from these Wwox LoF mice highlighted widespread changes in neuronal and glial pathways, enrichment of bioprocesses related to neuroinflammation and severe cerebellar dysfunction, activation of pathways compatible with compensatory neurogenesis along with major suppression of gene networks associated with neuronal cell differentiation and brain development. Our results show significant pathobiological effects and potential mechanisms through which Wwox LoF leads to cerebellar neurodegeneration, neuroinflammation, and ataxia.
2023-02-28 | GSE215425 | GEO
Project description:Wwox knockdown in Drosophila melanogaster neurons (elav-GAL4) also expressing human AB42 worsens lifespan and climbing as well as increasing AB42 load. To understand these effects further we performed transcriptomics on the same genotypes. Neurons expressing RNAi Control and a LacZ control, RNAi Control and AB42, Wwox RNAi and LacZ control or Wwox RNAi and AB42. This design allowed us to pull apart the effects of knockdown, amyloid and the interaction between the two.
2025-04-18 | E-MTAB-14948 | biostudies-arrayexpress
Project description:The aim of the current study was to investigate how various levels of WWOX, AP-2α and AP-2γ affect signaling pathways in bladder cancer cell lines. Global transcriptome analysis using CAGE-seq was conducted.
2022-01-17 | GSE193659 | GEO
Project description:WWOX expression is lost during tumor progression in many human malignancies including breast cancer. To understand the effects of loss of WWOX expression we analyzed the consequences of its silencing in normal human breast cells (MCF10F). WWOX silencing led to the formation of larger cell colonies, increased cell motility and decreased cell attachment. WWOX silenced cells demonstrated deregulated expression on genes involved in cell cycle, DNA damage response and cell motility. We detected an enrichment of targets activated by the SMAD3 transcription factor. Most notably expression of ANGPTL4, FST, PTHLH and SERPINE1 were all significantly increased upon WWOX silencing. Upregulation of these genes can be reversed by re-expressing WWOX in the previously silenced cells thus suggesting an inverse correlation between WWOX protein expression and SMAD3 transcriptional activity. Importantly, we demonstrate that WWOX physically interacts with SMAD3 protein via WW domain 1, that WWOX expression dramatically decreases SMAD3 occupancy at the ANGPTL4 and SERPINE1 promoters and significantly quenches activation of a TGFβ responsive reporter (3TP-LUX). Furthermore, WWOX expression leads to intracellular redistribution of SMAD3 protein levels redirecting protein availability from the nuclear to the cytoplasmic compartment. Interestingly, meta-analysis of gene expression breast cancer datasets indicate that WWOX and ANGPTL4 expression, encoding a secreted protein of key relevance in breast cancer lung metastatic cells, are inversely correlated and the WWOXlo/ANGPTL4hi cluster of tumors are enriched in triple-negative and basal-like sub-types. In summary, we demonstrate that WWOX modulates SMAD3 signaling in breast cells via direct WW-domain binding and potential cytoplasmic sequestration of SMAD3 protein. Since loss of WWOX expression increases with breast cancer progression and it behaves as an inhibitor of SMAD3 transcriptional activity these observations may help explain, at least in part, the paradoxical pro-tumorigenic effects of TGFβ signaling in advanced breast cancer.
2013-11-28 | GSE47371 | GEO
Project description:The WWOX gene is known for its tumor suppressor character and seems to be one of the main cellular regulators of cell cycle and apoptosis. The aim of the study was to identify cellular pathways and biological processes influenced by WWOX in glioblastoma cells. Our experiment showed that in this type of cancer WWOX, beside cell cycle and apoptosis control, may be involved in metabolism, cytoskeleton structure and differentiation.
2013-10-22 | GSE51481 | GEO