Literature DB >> 29387236

Expression profile and clinical significance of Wnt signaling in human gliomas.

Hao Zhang1, Yanhua Qi1, Decheng Geng1, Yi Shi1, Xu Wang1, Rutong Yu2,3, Xiuping Zhou2,3.   

Abstract

Wnt signaling has been identified as a critical regulator of human tumor development in vitro. However, there remains a lack of studies systematically examining the expression pattern and clinical relevance of the core molecules of Wnt signaling in glioma tissues. In the present study, it was identified that the mRNA expression levels of Wnt3a and 5a, and their receptors frizzled 2, 6 and 7 increased, whereas Wnt7b was markedly decreased in glioma relative to non-tumor tissue. The mRNA levels of β-catenin, adenomatous polyposis coli gene product, glycogen synthase kinase 3β (GSK3β) and AXIN1 and its target genes cyclin D1 and AXIN2 did not differ. Similarly, the protein levels of Wnt2b, 3a and 5a were increased in gliomas, while β-catenin, GSK3β and cyclin D1 were not. Furthermore, based on data from the R2: Genomics Analysis and Visualization Platform, the expression of Wnt2b and 5a, and frizzled 2, 6 and 7 were highly associated with the prognosis of patients with glioma. Taken together, the results of the present study demonstrate that β-catenin is not upregulated in gliomas and that the Wnt signaling pathway may promote glioma development via noncanonical or alternative pathways.

Entities:  

Keywords:  Wnt/β-catenin; cyclin D1; glioma; glycogen synthase kinase 3β

Year:  2017        PMID: 29387236      PMCID: PMC5768065          DOI: 10.3892/ol.2017.7315

Source DB:  PubMed          Journal:  Oncol Lett        ISSN: 1792-1074            Impact factor:   2.967


  49 in total

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Journal:  Science       Date:  2015-09-18       Impact factor: 47.728

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4.  Long noncoding RNA OIP5-AS1 targets Wnt-7b to affect glioma progression via modulation of miR-410.

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7.  Conditional Deletion of Foxg1 Alleviates Demyelination and Facilitates Remyelination via the Wnt Signaling Pathway in Cuprizone-Induced Demyelinated Mice.

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