Document Detail


Epithelial-mesenchymal transitions in cancer progression.
MedLine Citation:
PMID:  9124038     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Epithelial cells are the most important cell type in the development of human malignancies. More than 90% of all malignant tumors are carcinomas, and thus of epithelial origin. Aberrant growth and the ability to invade the underlying tissues are intrinsic properties of the fatally altered cells. Multiple genetic alterations that can influence growth and genetic stability of the carcinoma cells have been characterised during tumor progression. Loss of epithelial morphology and the acquisition of mesenchymal characteristics are typical for carcinoma cells late in tumor progression and correlate with metastatic potential. In vitro, epithelial-mesenchymal transitions can be induced by interference with the integrity of the adherens junction, by signalling via tyrosine kinases, and by oncogene expression. In carcinoma cells, loss or downregulation of E-cadherin expression are frequently observed in carcinomas, and correlate with the malignancy of the tumor. In general, this change in expression is regulated at the transcriptional level. However, tumor types or cell lines exist which show mesenchymal characteristics but nevertheless express E-cadherin protein or mRNA. A more-detailed analysis demonstrated that other mechanisms that interfere with E-cadherin-mediated cell adhesion can be operative. Mutations in the E-cadherin gene and loss or mutation of the second, intact copy as well as mutation in the catenin genes, which encode proteins that interact with the cytoplasmic portion of E-cadherin, can be observed. In addition, transient or unregulated phosphorylation by receptor tyrosine kinases or oncogenic tyrosine kinases, respectively, can interfere with the epithelial morphology and induce a mesenchymal conversion. Since tyrosine phosphorylation of beta-catenin correlates with the epithelial-mesenchymal transition that is observed, E-cadherin-mediated cell adhesion might be modulated by such a mechanism. Interestingly, the same molecules implicated in the control of malignant properties turn out to play fundamental roles in the control of normal epithelial growth, differentiation and morphogenesis.
Authors:
C Birchmeier; W Birchmeier; B Brand-Saberi
Related Documents :
11180088 - Cd44 variant overexpression in gallbladder carcinoma associated with tumor dedifferenti...
15848738 - Clear cell renal cell carcinoma.
11170298 - Tgf-beta in uveal melanoma.
10029078 - Suppression of angiogenesis, tumorigenicity, and metastasis by human prostate cancer ce...
10587238 - Boron self-shielding effects on dose delivery of neutron capture therapy using epitherm...
10201598 - Sclerosing sweat duct carcinoma of the eyelid margin: unusual presentation of a rare tu...
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Acta anatomica     Volume:  156     ISSN:  0001-5180     ISO Abbreviation:  Acta Anat (Basel)     Publication Date:  1996  
Date Detail:
Created Date:  1997-04-24     Completed Date:  1997-04-24     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0370272     Medline TA:  Acta Anat (Basel)     Country:  SWITZERLAND    
Other Details:
Languages:  eng     Pagination:  217-26     Citation Subset:  IM    
Affiliation:
Department of Medical Genetics, Max-Delbrueck Zentrum, für molekulare Medizin, Berlin, Germany.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Cadherins / biosynthesis
Carcinoma / pathology,  physiopathology*,  secondary
Disease Progression
Epithelium / physiology,  ultrastructure
Hepatocyte Growth Factor / physiology
Humans
Mesoderm / physiology*,  ultrastructure
Morphogenesis
Neoplasms / pathology,  physiopathology*
Proto-Oncogene Proteins c-met
Receptor Protein-Tyrosine Kinases / metabolism,  physiology
Chemical
Reg. No./Substance:
0/Cadherins; 67256-21-7/Hepatocyte Growth Factor; EC 2.7.10.1/Proto-Oncogene Proteins c-met; EC 2.7.10.1/Receptor Protein-Tyrosine Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Epithelial-mesenchymal transition during trophoblast differentiation.
Next Document:  Model systems of epithelium-mesenchyme transitions.