University of Cambridge > Talks.cam > Cellular Genetic Disease Seminar > Caspase-2 as a tumour suppressor.

Caspase-2 as a tumour suppressor.

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  • UserProfessor Sharad Kumar, Senior Principal Research Fellow of the NHMRC Australia, a Co-Founder and Co-Director of the Centre for Cancer Biology, a Professor of Cell Biology and the Chair of Cancer Biology at the University of South Australia
  • ClockWednesday 03 July 2019, 12:30-13:30
  • HouseDixon Greaves Room, Department of Pathology, Tennis Court Road.

If you have a question about this talk, please contact Emma Copley.

Host: Ivano Amelio (ia348@mrc-tox.cam.ac.uk) please contact Ivano if you would like to speak to Professor Kumar after his seminar. (Tea and coffee offered at 1215)

Caspase-2, the most evolutionarily conserved member of the caspase family, has redundant function in cell death during development. Our recent work suggests that caspase-2 is a tumour suppressor as caspase-2 deficiency enhances tumourigenesis in several mouse models. Interestingly caspase-2-deficient tumours always show enhanced chromosomal instability (CIN) and aneuploidy. Increased CIN and aneuploidy are also characteristics of caspase-2-deficient mouse embryonic fibroblasts in culture as well as human tumour cells with CASP2 gene knockout. We further found that caspase-2 is required for apoptotic deletion of cells carrying mitotic defects. Thus apoptotic activity of caspase-2 is necessary for deleting cells with CIN to limit aneuploidy and we propose that this is linked to the tumour suppressor function of caspase-2. Other recent studies have suggested that in response of cytokinesis failure caspase-2-mediates cleavage of Mdm2 that results in p53 stabilization and cell cycle arrest, thus preventing polyploidy. It is therefore possible that caspase-2 is involved in two checkpoints, one leading to apoptosis of cells with CIN and the other, cell cycle arrest following cytokinesis failure. We are now investigating how caspase-2 senses mitotic errors and becomes activated and how is such activation regulated.

This talk is part of the Cellular Genetic Disease Seminar series.

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