Epidermal growth factor-induced epithelio-mesenchymal transition in human breast carcinoma cells

Ackland, Leigh, Newgreen, Donald, Fridman, Masha, Waltham, Mark, Arvanitis, Angela, Minichiello, Joseph, Price, John and Thompson, Erik 2003, Epidermal growth factor-induced epithelio-mesenchymal transition in human breast carcinoma cells, Laboratory investigation, vol. 83, no. 3, pp. 435-448.

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Title Epidermal growth factor-induced epithelio-mesenchymal transition in human breast carcinoma cells
Author(s) Ackland, LeighORCID iD for Ackland, Leigh orcid.org/0000-0002-7474-6556
Newgreen, Donald
Fridman, Masha
Waltham, Mark
Arvanitis, Angela
Minichiello, Joseph
Price, John
Thompson, Erik
Journal name Laboratory investigation
Volume number 83
Issue number 3
Start page 435
End page 448
Publisher United States and Canadian Academy of Pathology
Place of publication Baltimore, Md.
Publication date 2003-03
ISSN 0023-6837
Summary PMC42-LA cells display an epithelial phenotype: the cells congregate into pavement epithelial sheets in which E-cadherin and beta-catenin are localized at cell-cell borders. They abundantly express cytokeratins, although 5% to 10% of the cells also express the mesenchymal marker vimentin. Stimulation of PMC42-LA cells with epidermal growth factor (EGF) leads to epithelio-mesenchymal transition-like changes including up-regulation of vimentin and down-regulation of E-cadherin. Vimentin expression is seen in virtually all cells, and this increase is abrogated by treatment of cells with an EGF receptor antagonist. The expression of the mesenchyme-associated extracellular matrix molecules fibronectin and chondroitin sulfate proteoglycan also increase in the presence of EGF. PMC42-LA cells adhere rapidly to collagen I, collagen IV, and laminin-1 substrates and markedly more slowly to fibronectin and vitronectin. EGF increases the speed of cell adhesion to most of these extracellular matrix molecules without altering the order of adhesive preference. EGF also caused a time-dependent increase in the motility of PMC42-LA cells, commensurate with the degree of vimentin staining. The increase in motility was at least partly chemokinetic, because it was evident both with and without chemoattractive stimuli. Although E-cadherin staining at cell-cell junctions disappeared in response to EGF, beta-catenin persisted at the cell periphery. Further analysis revealed that N-cadherin was present at the cell-cell junctions of untreated cells and that expression was increased after EGF treatment. N- and E-cadherin are not usually coexpressed in human carcinoma cell lines but can be coexpressed in embryonic tissues, and this may signify an epithelial cell population prone to epithelio-mesenchymal-like responses.
Language eng
Field of Research 060106 Cellular Interactions (incl Adhesion, Matrix, Cell Wall)
Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences
HERDC Research category C1 Refereed article in a scholarly journal
Copyright notice ©2003, United States and Canadian Academy of Pathology
Persistent URL http://hdl.handle.net/10536/DRO/DU:30002075

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