title: Loss of expression and altered localization of KAI1 and CD9 protein are associated with epithelial ovarian cancer progression.
abstract: OBJECTIVE
  Impairment of cell adhesion plays a vital role in tumor progression. E- and N-cadherin, CD9, and KAI1 are all adhesion molecules that have been implicated in the progression of several different tumor types. To help explain the potential role these adhesion molecules have in ovarian cancer, comparisons were made between expression patterns in normal ovary and various grades of primary and metastatic epithelial ovarian cancers.
  
  
  METHODS
  Thirty-two primary and 8 metastatic human ovarian epithelial carcinomas and 18 samples of normal ovarian tissue were examined for adhesion molecule expression using immunohistochemistry.
  
  
  RESULTS
  KAI1 and CD9 revealed an inverse relationship between tumor grade and expression levels, characterized by high expression in low-grade tumors and low expression in high-grade tumors and metastases. KAI1 and CD9 also demonstrated a shift in cellular localization from the membrane in grade 1 tumors to the cytoplasm in grade 3 tumors. N-cadherin expression showed a positive trend between expression levels and tumor grade. E-cadherin expression varied little between different tumor grades and metastases. Inclusion cysts (n = 6) and surface invaginations often strongly expressed KAI1, CD9, and E-cadherin. KAI1 expression was variable in ovarian follicles and corpora lutea depending on their stage of development.
  
  
  CONCLUSIONS
  Although sample size is limited, these findings suggest that progression of ovarian epithelial carcinomas is associated with down-regulation and altered cellular localization of KAI1 and CD9. In addition, variable KAI1 expression during follicular and luteal development suggests that it has a physiological function in the ovary. Further investigation will be needed to see if it is also regulated this way during progression of ovarian cancers.
authors.affiliation: Laboratory of Women's Health, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.
authors.forename: Christopher D
authors.initials: CD
authors.lastname: Houle
authors.forename: Xiao-Yu
authors.initials: XY
authors.lastname: Ding
authors.forename: Julie F
authors.initials: JF
authors.lastname: Foley
authors.forename: Cynthia A
authors.initials: CA
authors.lastname: Afshari
authors.forename: J Carl
authors.initials: JC
authors.lastname: Barrett
authors.forename: Barbara J
authors.initials: BJ
authors.lastname: Davis
mesh_terms: D015703:Antigens, CD / Q000096:biosynthesis*; D015820:Cadherins / Q000096:biosynthesis; D018450:Disease Progression; D015536:Down-Regulation; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D051861:Kangai-1 Protein; D008562:Membrane Glycoproteins / Q000096:biosynthesis*; D009362:Neoplasm Metastasis; D010051:Ovarian Neoplasms / Q000378:metabolism* / Q000473:pathology; D010053:Ovary / Q000378:metabolism; D011518:Proto-Oncogene Proteins; D060245:Tetraspanin 29
chemical_list: D015703:Antigens, CD; C497688:CD82 protein, human; C554869:CD9 protein, human; D015820:Cadherins; D051861:Kangai-1 Protein; D008562:Membrane Glycoproteins; D011518:Proto-Oncogene Proteins; D060245:Tetraspanin 29