Caspase 2 in mitotic catastrophe: The terminator of aneuploid and tetraploid cells. (4th May 2017)

• Record Type: Journal Article
• Authors: Vitale, Ilio; Manic, Gwenola; Castedo, Maria; Kroemer, Guido
• Is Part Of: Molecular & cellular oncology. Volume 4:Number 3(2017)
• Publication Date: 2017-05-04
• Subjects: Chromosome instability -- mitotic slippage -- polyploidy -- replication stress -- spindle assembly checkpoint -- targeted cancer therapy; Tumors -- Periodicals; Neoplasms; Periodicals; 616.99
• DOI: 10.1080/23723556.2017.1299274
• Languages: English
• ISSNs: 2372-3556

Abstract

ABSTRACT: Mitotic catastrophe is an oncosuppressive mechanism that targets cells experiencing defective mitoses via the activation of specific cell cycle checkpoints, regulated cell death pathways and/or cell senescence. This prevents the accumulation of karyotypic aberrations, which otherwise may drive oncogenesis and tumor progression. Here, we summarize experimental evidence confirming the role of caspase 2 (CASP2) as the main executor of mitotic catastrophe, and we discuss the signals that activate CASP2 in the presence of mitotic aberrations. In addition, we summarize the main p53-dependent and -independent effector pathways through which CASP2 limits chromosomal instability and non-diploidy, hence mediating robust oncosuppressive functions.