Gene Expression in Wilms Tumor: Disturbance of the Wnt Signaling Pathway and MicroRNA Biogenesis

Wilms Tumor ◽  
2016 ◽  
pp. 149-162
Author(s):  
Dirce Maria Carraro ◽  
◽  
Rodrigo F. Ramalho ◽  
Mariana Maschietto ◽  
◽  
...  
Keyword(s):  
Gene Expression ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Wilms Tumor ◽  
Wnt Signaling Pathway ◽  
Microrna Biogenesis

Molecular Profiling of Isolated Histological Components of Wilms Tumor Implicates a Common Role for the Wnt Signaling Pathway in Kidney and Tumor Development

Oncology ◽  
2008 ◽  
Vol 75 (1-2) ◽  
pp. 81-91 ◽  
Author(s):  
Mariana Maschietto ◽  
Beatriz de Camargo ◽  
Helena Brentani ◽  
Paul Grundy ◽  
Simone T. Sredni ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Signaling Pathway ◽  
Wilms Tumor ◽  
Wnt Signaling Pathway ◽  
Tumor Development ◽  
Molecular Profiling

scholarly journals Network analysis uncovers putative genes affecting resistance to tick infestation in Braford cattle skin

BMC Genomics ◽  
2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Daniela D. Moré ◽  
Fernando F. Cardoso ◽  
Maurício A. Mudadu ◽  
Wilson Malagó-Jr ◽  
Claudia C. Gulias-Gomes ◽  
...  
Keyword(s):  
Gene Expression ◽  
Network Analysis ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Tick Infestation ◽  
Wnt Signaling Pathway ◽  
Functional Enrichment ◽  
A Genome ◽  
Genetic Mechanisms ◽  
Different Levels

Abstract Background Genetic resistance in cattle is considered a suitable way to control tick burden and its consequent losses for livestock production. Exploring tick-resistant (R) and tick-susceptible (S) hosts, we investigated the genetic mechanisms underlying the variation of Braford resistance to tick infestation. Skin biopsies from four-times-artificially infested R (n = 20) and S (n = 19) hosts, obtained before the first and 24 h after the fourth tick infestation were submitted to RNA-Sequencing. Differential gene expression, functional enrichment, and network analysis were performed to identify genetic pathways and transcription factors (TFs) affecting host resistance. Results Intergroup comparisons of hosts before (Rpre vs. Spre) and after (Rpost vs. Spost) tick infestation found 51 differentially expressed genes (DEGs), of which almost all presented high variation (TopDEGs), and 38 were redundant genes. Gene expression was consistently different between R and S hosts, suggesting the existence of specific anti-tick mechanisms. In the intragroup comparisons, Rpost vs. Rpre and Spost vs. Spre, we found more than two thousand DEGs in response to tick infestation in both resistance groups. Redundant and non-redundant TopDEGs with potential anti-tick functions suggested a role in the development of different levels of resistance within the same breed. Leukocyte chemotaxis was over-represented in both hosts, whereas skin degradation and remodeling were only found in TopDEGs from R hosts. Also, these genes indicated the participation of cytokines, such as IL6 and IL22, and the activation of Wingless (WNT)-signaling pathway. A central gene of this pathway, WNT7A, was consistently modulated when hosts were compared. Moreover, the findings based on a genome-wide association study (GWAS) corroborate the prediction of the WNT-signaling pathway as a candidate mechanism of resistance. The regulation of immune response was the most relevant pathway predicted for S hosts. Members of Ap1 and NF-kB families were the most relevant TFs predicted for R and S, respectively. Conclusion This work provides indications of genetic mechanisms presented by Braford cattle with different levels of resistance in response to tick infestation, contributing to the search of candidate genes for tick resistance in bovine.

scholarly journals The Microphthalmia-Associated Transcription Factor Mitf Interacts with β-Catenin To Determine Target Gene Expression

2006 ◽  
Vol 26 (23) ◽  
pp. 8914-8927 ◽  
Author(s):  
Alexander Schepsky ◽  
Katja Bruser ◽  
Gunnar J. Gunnarsson ◽  
Jane Goodall ◽  
Jón H. Hallsson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Critical Role ◽  
Wnt Signaling Pathway ◽  
Feedback Mechanism ◽  
Canonical Wnt Signaling ◽  
Melanocyte Stem Cells ◽  
Canonical Wnt

ABSTRACT Commitment to the melanocyte lineage is characterized by the onset of expression of the microphthalmia-associated transcription factor (Mitf). This transcription factor plays a fundamental role in melanocyte development and maintenance and seems to be crucial for the survival of malignant melanocytes. Furthermore, Mitf has been shown to be involved in cell cycle regulation and to play important functions in self-renewal and maintenance of melanocyte stem cells. Although little is known about how Mitf regulates these various processes, one possibility is that Mitf interacts with other regulators. Here we show that Mitf can interact directly with β-catenin, the key mediator of the canonical Wnt signaling pathway. The Wnt signaling pathway plays a critical role in melanocyte development and is intimately involved in triggering melanocyte stem cell proliferation. Significantly, constitutive activation of this pathway is a feature of a number of cancers including malignant melanoma. Here we show that Mitf can redirect β-catenin transcriptional activity away from canonical Wnt signaling-regulated genes toward Mitf-specific target promoters to activate transcription. Thus, by a feedback mechanism, Mitf can diversify the output of canonical Wnt signaling to enhance the repertoire of genes regulated by β-catenin. Our results reveal a novel mechanism by which Wnt signaling and β-catenin activate gene expression, with significant implications for our understanding of both melanocyte development and melanoma.

scholarly journals Gene Expression Profiling of Peri-Implant Healing of PLGA-Li+ Implants Suggests an Activated Wnt Signaling Pathway In Vivo

PLoS ONE ◽  
2014 ◽  
Vol 9 (7) ◽  
pp. e102597 ◽  
Author(s):  
Anna Thorfve ◽  
Anna Bergstrand ◽  
Karin Ekström ◽  
Anders Lindahl ◽  
Peter Thomsen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Wnt Signaling ◽  
Gene Expression Profiling ◽  
Signaling Pathway ◽  
Expression Profiling ◽  
Wnt Signaling Pathway

scholarly journals The Wnt Signaling Pathway Effector TCF7L2 Controls Gut and Brain Proglucagon Gene Expression and Glucose Homeostasis

Diabetes ◽  
2012 ◽  
Vol 62 (3) ◽  
pp. 789-800 ◽  
Author(s):  
W. Shao ◽  
D. Wang ◽  
Y.-T. Chiang ◽  
W. Ip ◽  
L. Zhu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Glucose Homeostasis ◽  
Wnt Signaling Pathway

scholarly journals Colocalization and Redistribution of Dishevelled and Actin during WNT-Induced Mesenchymal Morphogenesis

2000 ◽  
Vol 149 (7) ◽  
pp. 1433-1442 ◽  
Author(s):  
Monica A. Torres ◽  
W. James Nelson
Keyword(s):  
Gene Expression ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Wnt Signaling Pathway ◽  
Cell Spreading ◽  
Mesenchymal Cell ◽  
Mouse Kidney ◽  
Cell Morphogenesis ◽  
Embryonic Mouse ◽  
Stimulation Of

Activation of the Wnt signaling pathway is important for induction of gene expression and cell morphogenesis throughout embryonic development. We examined the subcellular localization of dishevelled, the immediate downstream component from the Wnt receptor, in the embryonic mouse kidney. Using immunofluorescence staining, confocal microscopy, and coimmunoprecipitation experiments, we show that dishevelled associates with actin fibers and focal adhesion plaques in metanephric mesenchymal cells. Stimulation of Wnt signaling leads to profound changes in metanephric mesenchymal cell morphology, including disruption of the actin cytoskeleton, increased cell spreading, and increased karyokinesis. Upon activation of Wnt signaling, dishevelled also accumulates in and around the nucleus. Casein kinase Iε colocalizes with dishevelled along actin fibers and in the perinuclear region, whereas axin and GSK-3 are only present around the nucleus. These data indicate a branched Wnt signaling pathway comprising a canonical signal that targets the nucleus and gene expression, and another signal that targets the cytoskeleton and regulates cell morphogenesis.

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