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Journal ArticleDOI

Cadherins as modulators of cellular phenotype.

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TLDR
Cadherins have been implicated in a number of signaling pathways that regulate cellular behavior, and it is becoming increasingly clear that integration of information received from cell-cell signaling, cell-matrix signaling, and growth factor signaling determines ultimate cellular phenotype and behavior.
Abstract
Cadherins are transmembrane glycoproteins that mediate calcium-dependent cell-cell adhesion. The cadherin family is large and diverse, and proteins are considered to be members of this family if they have one or more cadherin repeats in their extracellular domain. Cadherin family members are the transmembrane components of a number of cellular junctions, including adherens junctions, desmosomes, cardiac junctions, endothelial junctions, and synaptic junctions. Cadherin function is critical in normal development, and alterations in cadherin function have been implicated in tumorigenesis. The strength of cadherin interactions can be regulated by a number of proteins, including the catenins, which serve to link the cadherin to the cytoskeleton. Cadherins have been implicated in a number of signaling pathways that regulate cellular behavior, and it is becoming increasingly clear that integration of information received from cell-cell signaling, cell-matrix signaling, and growth factor signaling determines ultimate cellular phenotype and behavior.

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Citations
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Focal adhesion kinase: in command and control of cell motility

TL;DR: A central question in cell biology is how membrane-spanning receptors transmit extracellular signals inside cells to modulate cell adhesion and motility.
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TGF-beta-induced epithelial to mesenchymal transition.

TL;DR: The induction of EMT in response to TGF-β is discussed, and the underlying signaling and transcription mechanisms are focused on.
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DeltaEF1 is a transcriptional repressor of E-cadherin and regulates epithelial plasticity in breast cancer cells.

TL;DR: RNA interference-mediated downregulation of deltaEF1 in cancer cells was sufficient to derepress E-cadherin expression and restore cell to cell adhesion, suggesting that deltaEF 1 is a key player in late stage carcinogenesis.
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E-cadherin, beta-catenin, and ZEB1 in malignant progression of cancer.

TL;DR: Mounting evidence indicates multiple reciprocal interactions of E-cadherin and β-catenin with EMT-inducing transcriptional repressors to stabilize an invasive mesenchymal phenotype of epithelial tumor cells.
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The transcription factor ZEB1 (δEF1) promotes tumour cell dedifferentiation by repressing master regulators of epithelial polarity

TL;DR: The data show that ZEB1 represents a key player in pathologic EMTs associated with tumour progression, and downregulation in undifferentiated cancer cells by RNA interference was sufficient to upregulate expression of cell polarity genes on the RNA and protein level, to re-establish epithelial features and to impair cell motility in vitro.
References
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Journal ArticleDOI

Epithelial–mesenchymal transitions in tumour progression

TL;DR: Epithelial–mesenchymal transition provides a new basis for understanding the progression of carcinoma towards dedifferentiated and more malignant states.
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The transcription factor Snail controls epithelial–mesenchymal transitions by repressing E-cadherin expression

TL;DR: It is shown that mouse Snail is a strong repressor of transcription of the E-cadherin gene, opening up new avenues for the design of specific anti-invasive drugs.
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The transcription factor snail is a repressor of E-cadherin gene expression in epithelial tumour cells.

TL;DR: It is shown that the transcription factor Snail, which is expressed by fibroblasts and some E-cadherin-negative epithelial tumour cell lines, binds to three E-boxes present in the human E-CADherin promoter and represses transcription of E- cadhersin.
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The cadherins: cell-cell adhesion molecules controlling animal morphogenesis.

TL;DR: It appears that each cadherin subclass has binding specificity and this molecular family is involved in selective cell-cell adhesion, indicating a crucial role in construction of tissues and the whole animal body.
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A causal role for E-cadherin in the transition from adenoma to carcinoma

TL;DR: It is demonstrated that loss of E-cadherin-mediated cell adhesion is one rate-limiting step in the progression from adenoma to carcinoma in a transgenic mouse model of pancreatic β-cell carcinogenesis.