Imperial College London

Dr Ernesto Yagüe

Faculty of MedicineDepartment of Surgery & Cancer

Non-Clinical Lecturer in Cancer Cell Biology
 
 
 
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Contact

 

+44 (0)20 7594 2802ernesto.yague Website

 
 
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Location

 

Cancer Research Centre, room 135ICTEM buildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Hu:2014:10.1007/s10549-013-2809-2,
author = {Hu, Y and Li, S and Yang, M and Yan, C and Fan, D and Zhou, Y and Zhang, Y and Yaguee, E and Xiong, D},
doi = {10.1007/s10549-013-2809-2},
journal = {Breast Cancer Research and Treatment},
pages = {287--299},
title = {Sorcin silencing inhibits epithelial-to-mesenchymal transition and suppresses breast cancer metastasis in vivo},
url = {http://dx.doi.org/10.1007/s10549-013-2809-2},
volume = {143},
year = {2014}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Sorcin, a 22-kDa calcium-binding protein, renders cancer cells resistant to chemotherapeutic agents, thus playing an important role in multidrug resistance. As there is a clear association between drug resistance and an aggressive phenotype, we asked whether sorcin affects also the motility, invasion, and stem cell characteristics of cancer cells. We have used both RNA interference (transient and stable expression of hairpins) and a lentiviral expression vector to experimentally modulate sorcin expression in a variety of cells. We demonstrate that sorcin depletion in MDA-MB-231 breast cancer cells reduces the pool of CD44+/CD24− and ALDH1high cancer stem cells (CSCs) as well as mammosphere-forming capacity. We also observe that sorcin regulates epithelial-mesenchymal transition and CSCs partly through E-cadherin and vascular endothelial growth factor expression. This leads to the acquisition of an epithelial-like phenotype, attenuating epithelial-mesenchymal transition and suppression of metastases in nude mice. The sorcin-depleted phenotype can also be reproduced in lung adenocarcinoma A549 cells and lung fibrosarcoma HT1080 cells. In addition, overexpression of sorcin in MCF7 cells, which have low endogenous sorcin expression levels, increases their migration and invasion in vitro. This offers the rationale for the development of therapeutic strategies down-regulating sorcin expression for the treatment of cancer.
AU - Hu,Y
AU - Li,S
AU - Yang,M
AU - Yan,C
AU - Fan,D
AU - Zhou,Y
AU - Zhang,Y
AU - Yaguee,E
AU - Xiong,D
DO - 10.1007/s10549-013-2809-2
EP - 299
PY - 2014///
SN - 0167-6806
SP - 287
TI - Sorcin silencing inhibits epithelial-to-mesenchymal transition and suppresses breast cancer metastasis in vivo
T2 - Breast Cancer Research and Treatment
UR - http://dx.doi.org/10.1007/s10549-013-2809-2
UR - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000329364200008&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR - http://hdl.handle.net/10044/1/69161
VL - 143
ER -