There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.
Most human cancers show chromosomal instability (CIN), but the precise mechanisms
remain uncertain. Annexin A2 is frequently overexpressed in human cancers, and its
relationship to tumorigenesis is poorly understood. We found that annexin A2 is overexpressed
in the nuclei of CIN cells compared with cells with microsatellite instability (MIN).
Ectopic annexin A2 expression in MIN cells results in a high level of aneuploidy and
induces lagging chromosomes; suppression of annexin A2 in CIN cells reduces such CIN
signatures with apoptosis of highly aneuploid cells. Ectopic expression of annexin
A2 in MIN cells reduces the expression of centromere proteins. Conversely, annexin
A2-knockdown in CIN cells increases the expression of centromere proteins. Moreover,
the endogenous expression levels of centromere proteins in CIN cells were greatly
reduced compared with MIN cell lines. The reduced expression of centromere proteins
likely occurred due to aberrant centromere localization of coilin, a major component
of the Cajal bodies. These results suggest that nuclear accumulation of annexin A2
has a crucial role in CIN by disrupting centromere function.