WT1 expression in breast cancer disrupts the epithelial-mesenchymal balance of tumour cells and correlates with the metabolic response to docetaxel.Reportar como inadecuado




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Reference: Artibani, M, Sims, AH, Slight, J et al., (2017). WT1 expression in breast cancer disrupts the epithelial/mesenchymal balance of tumour cells and correlates with the metabolic response to docetaxel. Scientific Reports, 7, 45255.Citable link to this page:

 

WT1 expression in breast cancer disrupts the epithelial/mesenchymal balance of tumour cells and correlates with the metabolic response to docetaxel.

Abstract: WT1 is a transcription factor which regulates the epithelial-mesenchymal balance during embryonic development and, if mutated, can lead to the formation of Wilms' tumour, the most common paediatric kidney cancer. Its expression has also been reported in several adult tumour types, including breast cancer, and usually correlates with poor outcome. However, published data is inconsistent and the role of WT1 in this malignancy remains unclear. Here we provide a complete study of WT1 expression across different breast cancer subtypes as well as isoform specific expression analysis. Using in vitro cell lines, clinical samples and publicly available gene expression datasets, we demonstrate that WT1 plays a role in regulating the epithelial-mesenchymal balance of breast cancer cells and that WT1-expressing tumours are mainly associated with a mesenchymal phenotype. WT1 gene expression also correlates with CYP3A4 levels and is associated with poorer response to taxane treatment. Our work is the first to demonstrate that the known association between WT1 expression in breast cancer and poor prognosis is potentially due to cancer-related epithelial-to-mesenchymal transition (EMT) and poor chemotherapy response.

Publication status:PublishedPeer Review status:Peer reviewedVersion:Publisher's versionDate of acceptance:2017-02-23 Funder: Breast Cancer Now   Funder: Medical Research Council   Funder: Biotechnology and Biological Sciences Research Council   Notes:© The Author(s) 2017. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

Bibliographic Details

Publisher: Nature Publishing Group

Publisher Website: http://www.nature.com/

Journal: Scientific Reportssee more from them

Publication Website: http://www.nature.com/srep

Volume: 7

Issue Date: 2017-03

pages:45255Identifiers

Doi: https://doi.org/10.1038/srep45255

Issn: 2045-2322

Uuid: uuid:314e89f9-43a1-4825-bdf7-5ef10842dcad

Urn: uri:314e89f9-43a1-4825-bdf7-5ef10842dcad

Pubs-id: pubs:687527 Item Description

Type: journal-article;

Language: eng

Version: Publisher's versionKeywords: Journal Article

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Autor: Artibani, M - Oxford, MSD, RDM, RDM Clinical Laboratory Sciences - - - Sims, AH - - - Slight, J - - - Aitken, S - - - Thornburn,

Fuente: https://ora.ox.ac.uk/objects/uuid:314e89f9-43a1-4825-bdf7-5ef10842dcad



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