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2015 ; 112
(ä): 353-82
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Adhesion in mammary development: novel roles for E-cadherin in individual and
collective cell migration
#MMPMID25733146
Shamir ER
; Ewald AJ
Curr Top Dev Biol
2015[]; 112
(ä): 353-82
PMID25733146
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Epithelial tissues are essential for barrier function, secretion, and regulation
of fluid transport. Their function requires cell polarity and cell-cell adhesion,
mediated through intercellular junctions. Conversely, disruption of adhesion and
polarity is thought to drive cancer progression. The mammary gland is an
important model for cell adhesion due to its postnatal hormonally regulated
development; ducts undergo branching morphogenesis in response to steroid
hormones during puberty. These hormonal signals induce a transition from simple
to stratified architecture, initiated by asymmetric luminal cell divisions.
Ductal elongation is accomplished by this multilayered, low-polarity epithelium,
and polarity is reestablished as elongation ceases. The requirement for cell
adhesion has been tested in 3D culture and in vivo, using gene deletion,
knockdown, and misexpression in both developmental and homeostatic contexts.
Attention has focused on E-cadherin, the major classical cadherin in luminal
epithelial cells. Classic studies revealed a requirement for E-cadherin during
lactation, and E-cadherin loss is widely posited to promote metastasis. However,
recent findings demonstrated a broader requirement for E-cadherin during
branching morphogenesis and homeostasis and also, surprisingly, in epithelial
dissemination. These studies suggest that long-standing models of the role of
adhesion in epithelial biology need to be revisited. Advances in inducible gene
expression and knockdown, CRISPR/Cas9 technology, and fluorescent labeling of
genetically modified cells offer the opportunity to test the roles of diverse
adhesion systems and to develop a mechanistic understanding of how cell adhesion
regulates development and cancer.
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