Journal
JOURNAL OF CELL SCIENCE
Volume 125, Issue 4, Pages 844-857Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.087668
Keywords
N-cadherin; Astrocyte; Glioma; Cell migration; Cell polarity
Categories
Funding
- Institut National du Cancer [2009-1-RT-05]
- Association pour la Recherche sur le Cancer
- Ministere de l'enseignement superieur et de la recherche
- Centre National de la Recherche Scientifique
- Institut Pasteur
- Association pour la Recherche sur le Cancer, La Ligue contre le Cancer
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Perturbation of cell polarity is a hallmark of cancer cells. In carcinomas, loss of epithelial E-cadherin contributes to the loss of cell polarity and promotes epithelial-mesenchymal transition and carcinoma infiltration. However, the contribution of classical cadherins to the development of non-epithelial tumours is less well documented. We investigated the impact of the level of N-cadherin expression on the polarity and migration of normal and tumour glial cells. Low levels of N-cadherin were frequently observed in human glioma samples and purified glioma cells. Using a wound-healing assay, we show that a decreased level of N-cadherin promotes a faster and less-directed migration both in normal and tumour cells. N-cadherin-mediated contacts control cell velocity and polarity through the regulation of focal adhesions. In cells expressing low levels of N-cadherin, small focal adhesions are present at the entire cell periphery of confluent cells and are not affected by wounding of the cell monolayer. Under these conditions, wound-induced integrin-mediated recruitment of the small GTPase Cdc42, activation of the Cdc42-mediated polarity pathway and centrosome reorientation do not occur. Re-expression of N-cadherin in gliomas restores cell polarity and strongly reduces cell velocity, suggesting that loss of N-cadherin could contribute to the invasive capacity of tumour astrocytes.
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