ArticleOncogene2015
Nuclear accumulation of annexin A2 contributes to chromosomal instability by coilin-mediated centromere damage.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- USP10/XAB2/ANXA2 axis promotes DNA damage repair to enhance chemoresistance to oxaliplatin in colorectal cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Coilin Affects the Prognosis of Hepatocellular Carcinoma Through Cell Cycle and Apoptosis.Journal of hepatocellular carcinoma · 2025Article
- Finding new roles of classic biomolecular condensates in the nucleus: Lessons from fission yeast.Cell insight · 2024Review
- The fission yeast ortholog of Coilin, Mug174, forms Cajal body-like nuclear condensates and is essential for cellular quiescence.Nucleic acids research · 2024Article
- Article
- Advances in cancer treatment: a new therapeutic target, Annexin A2.Journal of Cancer · 2021Review
- Selective imaging of solid tumours via the calcium-dependent high-affinity binding of a cyclic octapeptide to phosphorylated Annexin A2.Nature biomedical engineering · 2020Article
- High-affinity RNA targets of the Survival Motor Neuron protein reveal diverse preferences for sequence and structural motifs.Nucleic acids research · 2018Article
- Annexin A2-mediated cancer progression and therapeutic resistance in nasopharyngeal carcinoma.Journal of biomedical science · 2018Review
- Reactive oxygen species exert opposite effects on Tyr23 phosphorylation of the nuclear and cortical pools of annexin A2.Journal of cell science · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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