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Loss of Function of E-Cadherin in Embryonic Stem Cells and the Relevance toModels of Tumorigenesis

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JOURNAL OF ONCOLOGY
卷 2011, 期 -, 页码 -

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HINDAWI LTD
DOI: 10.1155/2011/352616

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  1. Biotechnology and Biological Sciences Research Council
  2. Engineering and Physical Sciences Research Council
  3. Technology Strategy Board
  4. Royal Society
  5. Association for International Cancer Research
  6. BBSRC [BB/E527239/1] Funding Source: UKRI
  7. EPSRC [TS/G000646/1] Funding Source: UKRI

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E-cadherin is the primary cell adhesion molecule within the epithelium, and loss of this protein is associated with amore aggressive tumour phenotype and poorer patient prognosis in many cancers. Loss of E-cadherin is a defining characteristic of epithelialmesenchymal transition (EMT), a process associated with tumour cell metastasis. We have previously demonstrated an EMT event during embryonic stem (ES) cell differentiation, and that loss of E-cadherin in these cells results in altered growth factor response and changes in cell surface localisation of promigratory molecules. We discuss the implication of loss of E-cadherin in ES cells within the context of cancer stem cells and current models of tumorigenesis. We propose that aberrant E-cadherin expression is a critical contributing factor to neoplasia and the early stages of tumorigenesis in the absence of EMT by altering growth factor response of the cells, resulting in increased proliferation, decreased apoptosis, and acquisition of a stem cell-like phenotype.

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