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J Biol Chem, Vol. 274, Issue 9, 5443-5453, February 26, 1999
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From the Glucocorticoid hormones, which are physiological
regulators of mammary epithelium development, induce the formation of
tight junctions in rat Con8 mammary epithelial tumor cells. We have discovered that, as part of this process, the synthetic glucocorticoid dexamethasone strongly and reversibly down-regulated the expression of
fascin, an actin-bundling protein that also interacts with the adherens
junction component Department of Molecular and Cell Biology and
the Cancer Research Laboratory, University of California, Berkeley,
California 94720-3200 and the § Department of Biochemistry
and Molecular Biology, University of Texas M.D. Anderson Cancer Center,
Houston, Texas 77030-4095
-catenin. Ectopic constitutive expression of
full-length mouse fascin containing a Myc epitope tag (Myc-fascin) in
Con8 cells inhibited the dexamethasone stimulation of transepithelial
electrical resistance, disrupted the induced localization of the tight
junction protein occludin and the adherens junction protein -catenin
to the cell periphery, and prevented the rearrangement of the actin
cytoskeleton. Ectopic expression of either the carboxyl-terminal 213 amino acids of fascin, which includes the actin and -catenin-binding
sites, or the amino-terminal 313 amino acids of fascin failed to
disrupt the glucocorticoid induction of tight junction formation.
Mammary tumor cells expressing the full-length Myc-fascin remained
generally glucocorticoid responsive and displayed no changes in the
levels or protein-protein interactions of junctional proteins or the
amount of cytoskeletal associated actin filaments. However, a cell
aggregation assay demonstrated that the expression of Myc-fascin
abrogated the dexamethasone induction of cell-cell adhesion. Our
results implicate the down-regulation of fascin as a key intermediate
step that directly links glucocorticoid receptor signaling to the
coordinate control of junctional complex formation and cell-cell
interactions in mammary tumor epithelial cells.
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