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Pushed out of a tough crowd: centrosome aberrations promote invasiveness

Lauren T Evans, View ORCID ProfileAndrew J Holland
DOI 10.15252/embj.201899422 | Published online 05.04.2018
The EMBO Journal (2018) e99422
Lauren T Evans
Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
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Andrew J Holland
Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
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Author Affiliations

  1. Lauren T Evans1 and
  2. Andrew J Holland (aholland@jhmi.edu)1
  1. 1Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD, USA
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Centrosome defects are observed in a broad array of solid and liquid tumors and are associated with advanced disease and poor patient prognosis. Unexpectedly, centrosome aberrations are present in only a subset of cells within a tumor and are poorly tolerated in non‐transformed cells, raising the conundrum of why centrosome aberrations are maintained during tumor evolution. New work by Ganier et al published in The EMBO Journal shows that centrosome defects can function in a non‐cell‐autonomous manner to force mitotic cells out of an epithelium, providing a plausible mechanism to promote dissemination of metastatic cells.

See also: O Ganier et al

The EMBO Journal (2018) e99422

Centrosomes are the major microtubule organizing centers of mammalian cells and play a key role in most microtubule‐related processes, including organizing cell shape and polarity, and guiding formation of a bipolar spindle during mitosis. To coordinate these processes, centrosome number and function must be controlled within the cell division cycle. Cells begin the cycle with a single centrosome that duplicates exactly once, to ensure cells have two copies of this organelle when they divide (Nigg & Holland, 2018). The two centrosomes then instruct the formation of a bipolar mitotic spindle, upon which the chromosomes are segregated. Centrosome aberrations are frequent in human tumors and can be subdivided into either numerical or structural alterations. Numerical alterations reflect increases in the number of centrosomes and are able to promote mitotic chromosome segregation errors that are sufficient to drive spontaneous tumor development in mice (Levine et al, 2017). On the other hand, structural defects encompass alterations in centrosomes shape and size. Although conceptually distinct, numerical …

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In this Issue
Volume 37, Issue 8
13 April 2018 | pp -
The EMBO Journal: 37 (8)
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