title: The role of claudin-1 and claudin-7 in cervical tumorigenesis.
abstract: OBJECTIVE
  The claudin family of proteins are key constituents of tight junctions and the aberrant expression of these proteins can contribute to de-stabilisation of tight junctions and thus to loss of cell polarity and cohesion. Increased expression of claudin-1 and claudin-7 has been observed in pre-invasive cervical lesions and cervical carcinomas. The present study attempted to assess the effect of claudin-1 and claudin-7 overexpression on the HeLa cervical carcinoma cell line, in terms of cell proliferation/viability, permeability, invasion and migration.
  
  
  METHODS
  HeLa cells were stably transfected with expression vectors containing the claudin-1 and claudin-7 genes to produce two separate stable cell lines expressing claudin-1 and claudin-7, respectively. The stable cell lines were examined with regard to their invasion and migration abilities, cell permeability and cell proliferation/viability and compared to non-claudin-1 or -7 transfected HeLa.
  
  
  RESULTS
  The present study found that claudin-1 and claudin-7 affected the migratory ability of HeLa cells, reducing their ability to migrate in a gap closure assay compared to non-claudin-transfected HeLa cells. Monolayers of claudin-1 and claudin-7 transfected cells also displayed an increased transepithelial electrical resistance indicating decreased permeability compared to non-claudin-transfected HeLa. The study found that claudin-1 or claudin-7 expression had no effect on the proliferation or viability of HeLa cells. Claudin-1 or -7 expression also did not affect the invasive ability of HeLa cells with both stable cells lines and non-claudin-transfected HeLa cells all showing low invasive ability.
  
  
  CONCLUSIONS
  The results of the present study indicate that claudin-1 and claudin-7 overexpression alone does not contribute to increased tumorigenesis in cervical carcinoma, instead claudin-1 and - 7 expression in HeLa cells contribute to reducing the migratory ability of cells and decrease their permeability.
authors.affiliation: School of Biological Sciences, Dublin Institute of Technology, Dublin, Ireland ciaran.cunniffe@student.dit.ie.
authors.forename: Ciaran
authors.initials: C
authors.lastname: Cunniffe
authors.affiliation: School of Biological Sciences, Dublin Institute of Technology, Dublin, Ireland.
authors.forename: Brenda
authors.initials: B
authors.lastname: Brankin
authors.affiliation: School of Biological Sciences, Dublin Institute of Technology, Dublin, Ireland.
authors.forename: Helen
authors.initials: H
authors.lastname: Lambkin
authors.affiliation: School of Biological Sciences, Dublin Institute of Technology, Dublin, Ireland.
authors.forename: Fergus
authors.initials: F
authors.lastname: Ryan
mesh_terms: D017209:Apoptosis; D015153:Blotting, Western; D002465:Cell Movement; D049109:Cell Proliferation; D062445:Claudin-1 / Q000235:genetics*; D057167:Claudins / Q000235:genetics*; D004553:Electric Conductivity; D005260:Female; D005434:Flow Cytometry; D005786:Gene Expression Regulation / Q000502:physiology*; D006367:HeLa Cells / Q000473:pathology; D006801:Humans; D019108:Tight Junctions; D014407:Tumor Cells, Cultured
chemical_list: C473255:CLDN7 protein, human; D062445:Claudin-1; D057167:Claudins
keywords: Cervical cancer; HPV; adhesion; claudins; tight junction