Literature DB >> 25246426

Wnt pathway in atypical teratoid rhabdoid tumors.

Madhavi Chakravadhanula1, Chris N Hampton1, Parth Chodavadia1, Victor Ozols1, Li Zhou1, Daniel Catchpoole1, Jingying Xu1, Anat Erdreich-Epstein1, Ratan D Bhardwaj1.   

Abstract

BACKGROUND: Atypical teratoid rhabdoid tumor (ATRT) is an aggressive pediatric brain tumor with limited therapeutic options. The hypothesis for this study was that the Wnt pathway triggered by the Wnt5B ligand plays an important role in ATRT biology. To address this hypothesis, the role of WNT5B and other Wnt pathway genes was analyzed in ATRT tissues and ATRT primary cell lines.
METHODS: Transcriptome-sequencing analyses were performed using nanoString platforms, immunohistochemistry, Western blotting, quantitative reverse transcriptase PCR, immunoprecipitation, short interference RNA studies, cell viability studies, and drug dose response (DDR) assays.
RESULTS: Our transcriptome-sequencing results of Wnt pathway genes from ATRT tissues and cell lines indicated that the WNT5B gene is significantly upregulated in ATRT samples compared with nontumor brain samples. These results also indicated a differential expression of both canonical and noncanonical Wnt genes. Imunoprecipitation studies indicated that Wnt5B binds to Frizzled1 and Ryk receptors. Inhibition of WNT5B by short interference RNA decreased the expression of FRIZZLED1 and RYK. Cell viability studies a indicated significant decrease in cell viability by inhibiting Frizzled1 receptor. DDR assays showed promising results with some inhibitors.
CONCLUSIONS: These promising therapeutic options will be studied further before starting a translational clinical trial. The success of these options will improve care for these patients.
© The Author(s) 2014. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Entities:  

Keywords:  ATRT; Frizzled 1; Ryk; Wnt pathway; Wnt5B

Mesh:

Substances:

Year:  2014        PMID: 25246426      PMCID: PMC4483069          DOI: 10.1093/neuonc/nou229

Source DB:  PubMed          Journal:  Neuro Oncol        ISSN: 1522-8517            Impact factor:   12.300


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