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  • CEP55 is a determinant of cell fate during perturbed mitosis in breast cancer

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    Author(s)
    Kalimutho, Murugan
    Sinha, Debottam
    Jeffery, Jessie
    Nones, Katia
    Srihari, Sriganesh
    Fernando, Winnie C
    Duijf, Pascal HG
    Vennin, Claire
    Raninga, Prahlad
    Nanayakkara, Devathri
    Mittal, Deepak
    Saunus, Jodi M
    Lakhani, Sunil R
    Lopez, J Alejandro
    Spring, Kevin J
    Timpson, Paul
    Gabrielli, Brian
    Waddell, Nicola
    Khanna, Kum Kum
    Griffith University Author(s)
    Lopez Ramirez, Alejandro
    Year published
    2018
    Metadata
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    Abstract
    The centrosomal protein, CEP55, is a key regulator of cytokinesis, and its overexpression is linked to genomic instability, a hallmark of cancer. However, the mechanism by which it mediates genomic instability remains elusive. Here, we showed that CEP55 overexpression/knockdown impacts survival of aneuploid cells. Loss of CEP55 sensitizes breast cancer cells to anti‐mitotic agents through premature CDK1/cyclin B activation and CDK1 caspase‐dependent mitotic cell death. Further, we showed that CEP55 is a downstream effector of the MEK1/2‐MYC axis. Blocking MEK1/2‐PLK1 signaling therefore reduced outgrowth of basal‐like syngeneic ...
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    The centrosomal protein, CEP55, is a key regulator of cytokinesis, and its overexpression is linked to genomic instability, a hallmark of cancer. However, the mechanism by which it mediates genomic instability remains elusive. Here, we showed that CEP55 overexpression/knockdown impacts survival of aneuploid cells. Loss of CEP55 sensitizes breast cancer cells to anti‐mitotic agents through premature CDK1/cyclin B activation and CDK1 caspase‐dependent mitotic cell death. Further, we showed that CEP55 is a downstream effector of the MEK1/2‐MYC axis. Blocking MEK1/2‐PLK1 signaling therefore reduced outgrowth of basal‐like syngeneic and human breast tumors in in vivo models. In conclusion, high CEP55 levels dictate cell fate during perturbed mitosis. Forced mitotic cell death by blocking MEK1/2‐PLK1 represents a potential therapeutic strategy for MYC‐CEP55‐dependent basal‐like, triple‐negative breast cancers.
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    Journal Title
    EMBO Molecular Medicine
    Volume
    10
    Issue
    9
    DOI
    https://doi.org/10.15252/emmm.201708566
    Copyright Statement
    © 2018 The Authors. This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
    Subject
    Biological sciences
    Other biological sciences not elsewhere classified
    Biomedical and clinical sciences
    Publication URI
    http://hdl.handle.net/10072/380951
    Collection
    • Journal articles

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