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First published online August 13, 2003

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Bcl-2 expressors lose touch

Bcl-2-family proteins ensure that cell proliferation and apoptosis are appropriately balanced in normal tissue homeostasis and development by controlling activation of the cell death effectors caspases. Dysregulation of the anti-apoptotic Bcl-2 is associated with loss of growth control in various tumours, and this is particularly evident in response to oestrogen in breast carcinoma. Manijeh Pasdar and co-workers now reveal another effect of Bcl-2: disruption of junctional complexes (see p. 3687). They show that, in MCF-7 breast carcinoma cells, Bcl-2 overexpression induces disappearance of the tight junctions, adherens junctions and desmosomes that normally link neighbouring cells. E-cadherins, associated catenins and the tight junction proteins ZO-1 and occludin all redistribute from the plasma membrane to the cytosol, and downregulation of Bcl-2 in response to oestrogen depletion reverses these effects. Interestingly, the authors find that Bcl-2 also causes ZO-1 to relocate to the nucleus, where, together with the transcription factor ZONAB, it upregulates expression of ErbB2 - a co-receptor for epidermal growth factor that downregulates E-cadherin expression. Since loss of contact inhibition can lead to unregulated growth, this could be an important consequence of Bcl-2 dysregulation that contributes to tumour malignancy.

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Bcl-2 expression decreases cadherin-mediated cell-cell adhesion

Laiji Li, Jody Backer, Annisa S. K. Wong, Erin L. Schwanke, Brian G. Stewart, and Manijeh Pasdar
JCS 2003 116: 3687-3700. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content