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The function of e-cadherin in stem cell pluripotency and self-renewal.

Soncin F, Ward CM - Genes (Basel) (2011)

Bottom Line: E-cadherin; pluripotency; embryonic stem cell; induced pluripotent stem cell; iPS; ES; signaling pathways; Activin; Nodal.

View Article: PubMed Central - PubMed

Affiliation: Core Technology Facility, Faculty of Medical and Human Sciences, The University of Manchester, 46 Grafton Street, M13 9NT, UK. fsoncin@sanfordburnham.org.

ABSTRACT
E-cadherin; pluripotency; embryonic stem cell; induced pluripotent stem cell; iPS; ES; signaling pathways; Activin; Nodal.

No MeSH data available.


Diagrammatic representation of the transcriptional and translational events associated with epithelial-mesenchymal transition during mouse and human ES cell differentiation. Undifferentiated ES cells exhibit E-cadherin-mediated cell-cell contact and this is associated with low levels of N-cadherin, E-cadherin repressors (Slug, Snail and SIP1) and matrix metalloproteinases (MMPs) [112,113]. Upon induction of ES cell differentiation, E-cadherin protein is rapidly lost from the cell surface and this is associated with increased N-cadherin, E-cadherin repressor (Slug, Snail and SIP1) and MMP expression [112,113]. Green denotes changes in both transcripts and protein; red denotes changes in transcripts only.
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f5-genes-02-00229: Diagrammatic representation of the transcriptional and translational events associated with epithelial-mesenchymal transition during mouse and human ES cell differentiation. Undifferentiated ES cells exhibit E-cadherin-mediated cell-cell contact and this is associated with low levels of N-cadherin, E-cadherin repressors (Slug, Snail and SIP1) and matrix metalloproteinases (MMPs) [112,113]. Upon induction of ES cell differentiation, E-cadherin protein is rapidly lost from the cell surface and this is associated with increased N-cadherin, E-cadherin repressor (Slug, Snail and SIP1) and MMP expression [112,113]. Green denotes changes in both transcripts and protein; red denotes changes in transcripts only.

Mentions: Regulation of E-cadherin expression is fundamental to vertebrate development [96]. E-cadherin is expressed in most adult epithelial tissues and has been shown to be a potent tumor invasion suppressor [105,106–108]. Loss of E-cadherin is associated with epithelial-mesenchymal transition (EMT), which is a crucial process in various stages of embryogenesis, tissue repair and tumor invasion [109,110]. EMT is characterized by loss of E-cadherin mediated cell-cell contact and acquisition of a more motile phenotype. Changes occurring during EMT comprise morphological modifications, altered cellular adhesion and motility, acquisition of anterior-posterior polarity, resistance to apoptosis and upregulation of matrix metalloproteinases [111]. EMT is characterized by a switch between E-cadherin, via upregulation of E-cadherin repressors (e.g., Slug and Snail), and a less adhesive cadherin, such as N-cadherin. During embryogenesis, regulation of E-cadherin and EMT is crucial for proper cell sorting, cell movement, polarity maintenance and barrier tissue formation. Our group has previously shown that ES cell differentiation is associated with an EMT-like event [112,113], and this is summarized in Figure 5. Loss of E-cadherin has been observed in many tumors of epithelial origin (e.g., gastric, gynecological and breast) and is often associated with EMT and poorer patient prognosis.


The function of e-cadherin in stem cell pluripotency and self-renewal.

Soncin F, Ward CM - Genes (Basel) (2011)

Diagrammatic representation of the transcriptional and translational events associated with epithelial-mesenchymal transition during mouse and human ES cell differentiation. Undifferentiated ES cells exhibit E-cadherin-mediated cell-cell contact and this is associated with low levels of N-cadherin, E-cadherin repressors (Slug, Snail and SIP1) and matrix metalloproteinases (MMPs) [112,113]. Upon induction of ES cell differentiation, E-cadherin protein is rapidly lost from the cell surface and this is associated with increased N-cadherin, E-cadherin repressor (Slug, Snail and SIP1) and MMP expression [112,113]. Green denotes changes in both transcripts and protein; red denotes changes in transcripts only.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3924836&req=5

f5-genes-02-00229: Diagrammatic representation of the transcriptional and translational events associated with epithelial-mesenchymal transition during mouse and human ES cell differentiation. Undifferentiated ES cells exhibit E-cadherin-mediated cell-cell contact and this is associated with low levels of N-cadherin, E-cadherin repressors (Slug, Snail and SIP1) and matrix metalloproteinases (MMPs) [112,113]. Upon induction of ES cell differentiation, E-cadherin protein is rapidly lost from the cell surface and this is associated with increased N-cadherin, E-cadherin repressor (Slug, Snail and SIP1) and MMP expression [112,113]. Green denotes changes in both transcripts and protein; red denotes changes in transcripts only.
Mentions: Regulation of E-cadherin expression is fundamental to vertebrate development [96]. E-cadherin is expressed in most adult epithelial tissues and has been shown to be a potent tumor invasion suppressor [105,106–108]. Loss of E-cadherin is associated with epithelial-mesenchymal transition (EMT), which is a crucial process in various stages of embryogenesis, tissue repair and tumor invasion [109,110]. EMT is characterized by loss of E-cadherin mediated cell-cell contact and acquisition of a more motile phenotype. Changes occurring during EMT comprise morphological modifications, altered cellular adhesion and motility, acquisition of anterior-posterior polarity, resistance to apoptosis and upregulation of matrix metalloproteinases [111]. EMT is characterized by a switch between E-cadherin, via upregulation of E-cadherin repressors (e.g., Slug and Snail), and a less adhesive cadherin, such as N-cadherin. During embryogenesis, regulation of E-cadherin and EMT is crucial for proper cell sorting, cell movement, polarity maintenance and barrier tissue formation. Our group has previously shown that ES cell differentiation is associated with an EMT-like event [112,113], and this is summarized in Figure 5. Loss of E-cadherin has been observed in many tumors of epithelial origin (e.g., gastric, gynecological and breast) and is often associated with EMT and poorer patient prognosis.

Bottom Line: E-cadherin; pluripotency; embryonic stem cell; induced pluripotent stem cell; iPS; ES; signaling pathways; Activin; Nodal.

View Article: PubMed Central - PubMed

Affiliation: Core Technology Facility, Faculty of Medical and Human Sciences, The University of Manchester, 46 Grafton Street, M13 9NT, UK. fsoncin@sanfordburnham.org.

ABSTRACT
E-cadherin; pluripotency; embryonic stem cell; induced pluripotent stem cell; iPS; ES; signaling pathways; Activin; Nodal.

No MeSH data available.