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Published online December 31, 2007
doi:10.1083/jcb.200706099
The Journal of Cell Biology, Vol. 179, No. 7, 1555-1567
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Pearson et al.
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Article

 Real-time imaging reveals that noninvasive mammary epithelial acini can contain motile cells

Gray W. Pearson and Tony Hunter

Molecular and Cell Biology Laboratory, Salk Institute, La Jolla, CA 92037

Correspondence to Tony Hunter: hunter{at}salk.edu

To determine how extracellular signal–regulated kinases (ERK) 1/2 promote mammary tumorigenesis, we examined the real-time behavior of cells in an organotypic culture of the mammary glandular epithelium. Inducible activation of ERK1/2 in mature acini elicits cell motility and disrupts epithelial architecture in a manner that is reminiscent of ductal carcinoma in situ; however, motile cells do not invade through the basement membrane and branching morphogenesis does not take place. ERK1/2-induced motility causes cells to move both within the cell monolayer that contacts the basement membrane surrounding the acinus and through the luminal space of the acinus. E-cadherin expression is reduced after ERK1/2 activation, but motility does not involve an epithelial–mesenchymal transition. Cell motility and the disruption of epithelial architecture require a Rho kinase– and myosin light chain kinase–dependent increase in the phosphorylation of myosin light chain 2. Our results identify a new mechanism for the disruption of architecture in epithelial acini and suggest that ERK1/2 can promote noninvasive motility in preinvasive mammary tumors.

Abbreviations used in this paper: 4-HT, 4-hydroxytamoxifen; DCIS, ductal carcinoma in situ; EMT, epithelial–mesenchymal transition; ERK, extracellular signal–regulated kinase; FMI, final mean intensity; HPV, human papillomavirus; MEK, MAPK/ERK kinase; MLC, myosin light chain; MLCK, MLC kinase; ROCK, Rho kinase.


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Motility without invasion
Nicole LeBrasseur
J. Cell Biol. 2007 179: 1327. [Full Text] [PDF]



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