Gene expression profiling of low-grade endometrial stromal sarcoma indicates fusion protein-mediated activation of the Wnt signaling pathway

2018 ◽  
Vol 149 (2) ◽  
pp. 388-393 ◽  
Author(s):  
Joanna Przybyl ◽  
Lukasz Kidzinski ◽  
Trevor Hastie ◽  
Maria Debiec-Rychter ◽  
Roel Nusse ◽  
...  
PLoS ONE ◽  
2014 ◽  
Vol 9 (7) ◽  
pp. e102597 ◽  
Author(s):  
Anna Thorfve ◽  
Anna Bergstrand ◽  
Karin Ekström ◽  
Anders Lindahl ◽  
Peter Thomsen ◽  
...  

PLoS ONE ◽  
2010 ◽  
Vol 5 (12) ◽  
pp. e15647 ◽  
Author(s):  
Magdalena Cizkova ◽  
Géraldine Cizeron-Clairac ◽  
Sophie Vacher ◽  
Aurélie Susini ◽  
Catherine Andrieu ◽  
...  

2007 ◽  
Vol 38 (1) ◽  
pp. 120-133 ◽  
Author(s):  
Zhao-Yang Zeng ◽  
Yan-Hong Zhou ◽  
Wen-Ling Zhang ◽  
Wei Xiong ◽  
Song-Qing Fan ◽  
...  

2010 ◽  
Vol 16 (7-8) ◽  
pp. 262-270 ◽  
Author(s):  
Ingrid Laurendeau ◽  
Marcela Ferrer ◽  
Delia Garrido ◽  
Nicky D’Haene ◽  
Patricia Ciavarelli ◽  
...  

BMC Genomics ◽  
2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Daniela D. Moré ◽  
Fernando F. Cardoso ◽  
Maurício A. Mudadu ◽  
Wilson Malagó-Jr ◽  
Claudia C. Gulias-Gomes ◽  
...  

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.


2006 ◽  
Vol 26 (23) ◽  
pp. 8914-8927 ◽  
Author(s):  
Alexander Schepsky ◽  
Katja Bruser ◽  
Gunnar J. Gunnarsson ◽  
Jane Goodall ◽  
Jón H. Hallsson ◽  
...  

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.


Sign in / Sign up

Export Citation Format

Share Document