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Metastasis

CAV1 connection

Nature Reviews Cancer volume 4, pages 90–91 (2004)Cite this article

During metastasis, changes in the tissue microenvironment allow cancer cells to escape the tumour and disseminate. Epidermal growth factor receptor (EGFR) overexpression and downregulation of E-cadherin — a key component of intercellular junctions — are both known to disrupt cell–cell interactions and, according to a report by Tony Hunter and colleagues in Cancer Cell, these processes are connected by the caveolae-associated protein caveolin-1 (CAV1). Not only does EGFR overexpression initially cause caveolin-dependent internalization of E-cadherin, it also ultimately reduces CAV1 protein levels, which activates the β-catenin signalling pathway and downregulates E-cadherin expression.

In response to EGF, EGFR-overexpressing cancer cells undergo an epithelial–mesenchymal transition, which is caused by loss of cell–cell junctions and cell depolarization. In A431 human cancer cells, rapid internalization of E-cadherin was associated with the early stages of this process and, as EGF is known to trigger CAV1 redistribution, the authors investigated whether the internalization was mediated by caveolae. Chemical depletion of cholesterol, a key component of caveolae, prevented E-cadherin internalization, indicating that caveolae are needed to downregulate surface E-cadherin and cause rapid loss of intercellular contacts.

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ORIGINAL RESEARCH PAPER

  1. Lu, Z., Ghosh, S., Wang, Z. & Hunter, T. Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of β-catenin, and enhanced tumor cell invasion. Cancer Cell 4, 499–515 (2003)

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  1. Emma Croager
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Croager, E. CAV1 connection. Nat Rev Cancer 4, 90–91 (2004). https://doi.org/10.1038/nrc1283

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  • DOI: https://doi.org/10.1038/nrc1283

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