Nuclear size normally scales with the size of the cell, but in cancer this ‘karyoplasmic ratio’ is disrupted. This is particularly so in more metastatic tumors where changes in the karyoplasmic ratio are used in both diagnosis and prognosis for several tumor types. However, the direction of nuclear size changes differs for particular tumor types: for example in breast cancer, larger nuclear size correlates with increased metastasis, while for lung cancer smaller nuclear size correlates with increased metastasis. Thus, there must be tissue-specific drivers of the nuclear size changes, but proteins thus far linked to nuclear size regulation are widely expressed. Notably, for these tumor types, ploidy changes have been excluded as the basis for nuclear size changes, and so, the increased metastasis is more likely to have a basis in the nuclear morphology change itself. We review what is known about nuclear size regulation and postulate how such nuclear size changes can increase metastasis and why the directionality can differ for particular tumor types.
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Cover Image
Cover Image
Cryo-electron microscopy density map of a Cowpea Mosaic virus (CPMV) empty virus-like particle (eVLP) at 2.7 Å resolution (EMD-3952). The large (L) subunit is displayed in green and the small (S) subunit in blue. Five S subunits interact to form pronounced turrets at the 5-fold axis. Here we show a view down a two-fold axis. The eVLP was produced by transient co-expression in plants of the precursor of the L and S subunits (VP60) and the virus-encoded protease (24K) required for its processing. For further details, please see article by Lomonossoff et al, pages 1263–1269
Breaking the scale: how disrupting the karyoplasmic ratio gives cancer cells an advantage for metastatic invasion
Andrea Rizzotto, Eric C. Schirmer; Breaking the scale: how disrupting the karyoplasmic ratio gives cancer cells an advantage for metastatic invasion. Biochem Soc Trans 15 December 2017; 45 (6): 1333–1344. doi: https://doi.org/10.1042/BST20170153
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