|Cancer||Cell death||Cell cycle||Cytoskeleton||Exo/endocytosis||Differentiation||Division||Organelles||Signalling||Stem cells||Trafficking|
Cell Biology International (2005) 29, 10121018 (Printed in Great Britain)
Mitotic catastrophe and endomitosis in tumour cells: An evolutionary key to a molecular solution
Jekaterina Erenpreisaa*, M. Kalejsa and M.S. Craggbc
aLab. Tum. Cell Biol., Biomedicine Centre of the Latvia University, Ratsupites 1, Riga LV-1067, Latvia
bUniversity of Southampton, Southampton, UK
cWEHI, Melbourne, Australia
Following genotoxic insult, p53 mutated tumour cells undergo mitotic catastrophe. This is characterised by a switch from mitosis to the endocycle. The essential difference between mitosis and the endocycle is that in the latter, DNA synthesis is uncoupled from cell division, which leads to the formation of endopolyploid cells. Recent data suggests that a return from the endocycle into mitosis is also possible. Furthermore, our observations indicate that a particular type of endocycle known as endomitosis may be involved in this return. Here we review the role of endomitosis in the somatic reduction of polyploidy during development and its postulated role in the evolution of meiosis. Finally, we incorporate these evolutionary data to help interpret our most recent observations in the tumour cell system, which indicate a role for endomitosis and meiotic regulators, in particular p39mos in the segregation of genomes (somatic reduction) of these endopolyploid cells.
Key words: Mitotic catastrophe, Tumours, Endomitosis, Somatic reduction, Meiotic regulators.
*Corresponding author. Tel.: +371 7 808 220; fax: +371 7 442 407.