Oncogenes and tumour suppressors take on centrosomes.
Chromosome instability, which is equated to mitotic defects and consequential chromosome segregation errors, provides a formidable basis for the acquisition of further malignant phenotypes during tumour progression. Centrosomes have a crucial role in the formation of bipolar mitotic spindles, which are essential for accurate chromosome segregation. Mutations of certain oncogenic and tumour-suppressor proteins directly induce chromosome instability by disrupting the normal function and numeral integrity of centrosomes. How these proteins control centrosome duplication and function, and how their mutational activation and/or inactivation results in numeral and functional centrosome abnormalities, is discussed in this Review.
Fukasawa
Kenji
K
Molecular Oncology Program, H. Lee Moffitt Cancer Center and Research Institute, Tampa, Florida 33612, USA. Kenji.Fukasawa@Moffitt.org
D021581:Active Transport, Cell Nucleus; D018385:Centrosome / Q000648:ultrastructure*; D043171:Chromosomal Instability / Q000235:genetics / Q000502:physiology; D056746:Cyclin G; D056766:Cyclin G1; D018844:Cyclin-Dependent Kinases / Q000378:metabolism; D016213:Cyclins / Q000378:metabolism; D004249:DNA Damage; D016147:Genes, Tumor Suppressor; D006801:Humans; D008938:Mitosis / Q000235:genetics / Q000502:physiology; D009154:Mutation; D009369:Neoplasms / Q000235:genetics* / Q000648:ultrastructure; D009857:Oncogenes / Q000235:genetics
C534702:CCNG1 protein, human; D056746:Cyclin G; D056766:Cyclin G1; D016213:Cyclins; D018844:Cyclin-Dependent Kinases