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@article{Rhys:2017:10.1083/jcb.201704102,
author = {Rhys, AD and Monteiro, P and Smith, C and Vaghela, M and Arnandis, T and Kato, T and Leitinger, B and Sahai, E and McAinsh, A and Charras, G and Godinho, SA},
doi = {10.1083/jcb.201704102},
journal = {Journal of Cell Biology},
pages = {195--209},
title = {Loss of E-cadherin provides tolerance to centrosome amplification in epithelial cancer cells},
url = {http://dx.doi.org/10.1083/jcb.201704102},
volume = {217},
year = {2017}
}

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TY  - JOUR
AB  - Centrosome amplification is a common feature of human tumors. To survive, cancer cells cluster extra centrosomes during mitosis, avoiding the detrimental effects of multipolar divisions. However, it is unclear whether clustering requires adaptation or is inherent to all cells. Here, we show that cells have varied abilities to cluster extra centrosomes. Epithelial cells are innately inefficient at clustering even in the presence of HSET/KIFC1, which is essential but not sufficient to promote clustering. The presence of E-cadherin decreases cortical contractility during mitosis through a signaling cascade leading to multipolar divisions, and its knockout promotes clustering and survival of cells with multiple centrosomes. Cortical contractility restricts centrosome movement at a minimal distance required for HSET/KIFC1 to exert its function, highlighting a biphasic model for centrosome clustering. In breast cancer cell lines, increased levels of centrosome amplification are accompanied by efficient clustering and loss of E-cadherin, indicating that this is an important adaptation mechanism to centrosome amplification in cancer.
AU  - Rhys,AD
AU  - Monteiro,P
AU  - Smith,C
AU  - Vaghela,M
AU  - Arnandis,T
AU  - Kato,T
AU  - Leitinger,B
AU  - Sahai,E
AU  - McAinsh,A
AU  - Charras,G
AU  - Godinho,SA
DO  - 10.1083/jcb.201704102
EP  - 209
PY  - 2017///
SN  - 0021-9525
SP  - 195
TI  - Loss of E-cadherin provides tolerance to centrosome amplification in epithelial cancer cells
T2  - Journal of Cell Biology
UR  - http://dx.doi.org/10.1083/jcb.201704102
UR  - http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000419133900020&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - http://hdl.handle.net/10044/1/58061
VL  - 217
ER  -

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