ArticleCancer science2013
Differences in the localization of the adenomatous polyposis coli-Asef/Asef2 complex between adenomatous polyposis coli wild-type and mutant cells.
Article in Cancer science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Mechanism of APC truncation involved in colorectal cancer tumorigenesis (Review).Oncology letters · 2025Review
- Review
- Asef controls vascular endothelial permeability and barrier recovery in the lung.Molecular biology of the cell · 2015Article
- Hepatocyte growth factor triggers distinct mechanisms of Asef and Tiam1 activation to induce endothelial barrier enhancement.Cellular signalling · 2014Article
- Differences in the localization of the adenomatous polyposis coli-Asef/Asef2 complex between adenomatous polyposis coli wild-type and mutant cells.Cancer science · 2013Article
- Adenomatous Polyposis Coli (APC) in cell migration.European journal of cell biologyReview
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tumor suppressor adenomatous polyposis coli (APC) is mutated in familial adenomatous polyposis and in many sporadic colorectal tumors. Adenomatous polyposis coli is known to negatively regulate Wnt signaling by inducing the degradation of β-catenin. Adenomatous polyposis coli also interacts with the guanine nucleotide exchange factors Asef and Asef2 and stimulates their activity, thereby regulating cell adhesion and migration. Here we show that in confluent, non-motile MDCK II cells, Asef/Asef2 are colocalized with APC at the sites of cell-cell adhesion at the apical and junctional levels. In contrast, in colorectal tumor cells containing mutated APC, significant amounts of Asef/Asef2 and the truncated mutant APCs are localized mainly in the cytoplasm. These results suggest that localization of the Asef/Asef2-APC complex at the sites of cell-cell contact is critical for the regulation of cell adhesion, and that the aberrant subcellular localization of these complexes in colorectal tumor cells may contribute to the cell's aberrant adhesive and migratory properties.
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Registered trials
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