Journal
CELL CYCLE
Volume 11, Issue 5, Pages 934-952Publisher
LANDES BIOSCIENCE
DOI: 10.4161/cc.11.5.19452
Keywords
MCT-1; p53; mitosis; centrosome; cytokinesis; nuclear abnormalities
Categories
Funding
- Wan Fang Hospital [100swf14]
- National Tsing Hua University
- National Health Research Institutes
- [MG-099-PP-05]
- [NSC96-2628-B-400-003-MY3]
- [NSC99-3112-B-400-002]
- [DOH100-TD-C-111-004]
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Centrosome amplification and chromosome abnormality are frequently identified in neoplasia and tumorigenesis. However, the mechanisms underlying these defects remain unclear. Here, we identify that MCT-1 is a centrosomal oncoprotein involved in mitosis. Knockdown of MCT-1 protein results in intercellular bridging, chromosome mis-congregation, cytokinesis delay and mitotic death. Introduction of MCT-1 oncogene into the p53 deficient cells (MCT-1-p53), the mitotic checkpoint kinases and proteins are deregulated synergistically. These biochemical alterations are accompanied with increased frequencies of cytokinesis failure, multi-nucleation and centrosome amplification in subsequent cell cycle. As a result, the incidences of polyploidy and aneuploidy are progressively induced by prolonged cell cultivation or further promoted by sustained spindle damage on MCT-1-p53 background. These data show that the oncoprotein perturbs centrosome structure and mitotic progression, which provide the molecular aspect of chromsomal abnormality in vitro and the information for understanding the stepwise progression of tumors under oncogenic stress.
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