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c-erbB2-induced epithelial-mesenchymal transition in mammary epithelial cells is suppressed by cell-cell contact and initiated prior to E-cadherin downregulation.

Journal article
Authors Lachmi E Jenndahl
Petter Isakson
Dan Baeckström
Published in International journal of oncology
Volume 27
Issue 2
Pages 439-48
ISSN 1019-6439
Publication year 2005
Published at Institute of Medical Biochemistry
Pages 439-48
Language en
Keywords Cadherins, metabolism, Cell Communication, physiology, Cell Count, Cell Line, Cell Proliferation, Cell Shape, physiology, Cell Survival, physiology, Down-Regulation, Epithelial Cells, cytology, drug effects, metabolism, Fibroblasts, cytology, drug effects, metabolism, Flow Cytometry, Humans, Mammary Glands, Human, cytology, metabolism, Mesoderm, cytology, metabolism, Nerve Growth Factor, pharmacology, Receptor, erbB-2, physiology, Signal Transduction, Time Factors
Subject categories Medical and Health Sciences


Prolonged signalling from the growth factor receptor subunit and proto-oncogene c-erbB2 has been shown to cause epithelial-mesenchymal transition (EMT) in mammary epithelial cells. Using a system where c-erbB2 homodimer signalling can be induced in human mammary epithelial cells, we characterised the properties of c-erbB2-induced EMT. The cells resulting from this transdifferentiation showed a pronounced and stable fibroblastic phenotype with spindle-like morphology, homogeneous high expression of vimentin, N-cadherin, and integrin alpha5 as well as loss of E-cadherin and desmoplakin. However, the rate at which EMT occurred was very slow compared to other reported systems, as complete conversion was not seen until after 12-15 weeks of c-erbB2 signalling. This time delay was however not due to the presence of long-lived intermediate cell types as measured by expression of combinations of markers. By studying morphological time-courses of individual colonies of epithelial cells subjected to c-erbB2 signalling, we could conclude that apart from EMT, c-erbB2 could also cause transition to very large cells retaining cell-cell contact but with little or no proliferative capacity. EMT preferentially occurred in small colonies, suggesting that extensive cell-cell contact inhibits EMT. When testing this conclusion by exposing cells to c-erbB2 signalling at different cell densities, we concluded that only cells kept at low density would undergo EMT. High cell density also prevented the proliferative decrease associated with prolonged c-erbB2 signalling. Immunofluorescence microscopy revealed that disruption of cell-cell contact was preceded by partial relocalisation of beta-catenin to the cytoplasm whereas downregulation of E-cadherin appeared to occur after initiation of cell scattering.

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