title: Epithelial to mesenchymal transition (EMT) seems to be regulated differently in endometriosis and the endometrium.
abstract: OBJECTIVE
  Epithelial-mesenchymal transition (EMT) endows cells with migratory and invasive properties, a prerequisite for the establishment of endometriotic lesions. However, the role EMT might play in the pathophysiology of endometriosis is still unknown. Therefore, we examined five recognized markers for EMT in endometrium and endometriosis: E-cadherin, N-cadherin, Twist, Snail and Slug.
  
  
  METHODS
  Immunohistochemistry was used for peritoneal, ovarian and rectovaginal endometriotic lesions (n = 27) and endometrium (n = 13). Reverse transcription polymerase chain reaction was applied to tissue samples and primary cell cultures of endometriotic lesions (n = 9) and endometrium (n = 8).
  
  
  RESULTS
  In endometriosis and endometrium E-cadherin, N-cadherin, Twist, Snail and Slug were expressed on protein and mRNA level. E-cadherin expression was strong in epithelial cells, but single E-cadherin-negative cells were frequently present in endometriosis. In endometriosis N-cadherin, Twist and Snail expression were upregulated in comparison with endometrium. The expression of E- and N-cadherin was inversely correlated, while that of N-cadherin and Twist was positively correlated.
  
  
  CONCLUSIONS
  This study strongly suggests that EMT may be regulated differently in endometriosis and the endometrium. Future research should further elucidate the regulation of EMT in the endometrium and endometriosis.
authors.affiliation: Department of Gynaecology, Endometriosis Research Centre Berlin, Charité Universitätsmedizin, Charitéplatz 1, 10117, Berlin, Germany, julia.bartley@charite.de.
authors.forename: J
authors.initials: J
authors.lastname: Bartley
authors.forename: A
authors.initials: A
authors.lastname: Jülicher
authors.forename: B
authors.initials: B
authors.lastname: Hotz
authors.forename: S
authors.initials: S
authors.lastname: Mechsner
authors.forename: H
authors.initials: H
authors.lastname: Hotz
mesh_terms: D000328:Adult; D015820:Cadherins / Q000235:genetics / Q000378:metabolism*; D002467:Cell Nucleus / Q000378:metabolism; D002478:Cells, Cultured; D003593:Cytoplasm / Q000378:metabolism; D004715:Endometriosis / Q000378:metabolism* / Q000473:pathology / Q000601:surgery; D004717:Endometrium / Q000378:metabolism* / Q000473:pathology / Q000601:surgery; D004847:Epithelial Cells / Q000378:metabolism; D058750:Epithelial-Mesenchymal Transition / Q000502:physiology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000071250:Snail Family Transcription Factors; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism*; D051879:Twist-Related Protein 1 / Q000235:genetics / Q000378:metabolism*
chemical_list: D015820:Cadherins; D012333:RNA, Messenger; C000604407:SNAI1 protein, human; D000071250:Snail Family Transcription Factors; D014157:Transcription Factors; D051879:Twist-Related Protein 1