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1: J Cell Biol. 2007 Dec 31;179(7):1555-67.
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Real-time imaging reveals that noninvasive mammary epithelial acini can contain motile cells.

Pearson GW, Hunter T.

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

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.

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PMID: 18166657 [PubMed - indexed for MEDLINE]

PMCID: PMC2373504