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
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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