title: The stimulation of IGF-1R expression by Lewis(y) antigen provides a powerful development mechanism of epithelial ovarian carcinoma.
abstract: OBJECTIVE
  This study aimed to measure and correlate the expression of insulin-like growth factor receptor-1 (IGF-1R) and the Lewis(y) antigen in ovarian cancer cell lines and tissue samples.
  
  
  METHODS
  Reverse transcriptase PCR (RT-PCR), Western blotting, immunoprecipitation, immunohistochemistry, and immunofluorescence double-labeling techniques were applied to detect and measure the expression of Lewis(y) and IGF-1R.
  
  
  RESULTS
  In α1,2-fucosyltransferase (α1,2-FT)-transfected cells, IGF-1R expression was significantly upregulated compared with cells that do not overexpress α1,2-FT (P < 0.05). The amount of Lewis(y) expressed on IGF-1R increased 1.81-fold in α1,2-FT-overexpressing cells (P < 0.05), but the ratio of Lewis(y) expressed on IGF-1R to total IGF-1R was unaltered between two cells (P > 0.05). In malignant epithelial ovarian tumors, the positivity rates of Lewis(y) and IGF-1R detection were 88.3% and 93.33%, respectively, which is higher than the positivity rates in marginal (60.00% and 63.33%, all P < 0.05), benign (33.00% and 53.33%, all P < 0.01), and normal (0% and 40%, all P < 0.01) ovarian samples. No correlations were detected in positivity rates of Lewis(y) or IGF-1R expression with respect to clinicopathological parameters in ovarian cancers (all P > 0.05). Both IGF-1R and Lewis(y) were highly expressed in ovarian cancer tissues, and their expression levels were positively correlated (P < 0.05).
  
  
  CONCLUSIONS
  Overexpression of Lewis(y) results in overexpression of IGF-1R. Both IGF-1R and Lewis(y) are associated with the occurrence and development of ovarian cancers.
authors.affiliation: Department of Obstetrics and Gynecology, Shengjing Hospital Affiliated to China Medical University, Shenyang 110004, China; E-Mails:  cyldw2007@163.com  (D.L.);  juanjuanliu_lg@yahoo.com.cn  (J.L.);  qingLiu@126.com  (Q.L.);  liushuicc@sina.com  (Y.H.);  zhangshl99@126.com  (S.Z.).
authors.forename: Dawo
authors.initials: D
authors.lastname: Liu
authors.forename: Juanjuan
authors.initials: J
authors.lastname: Liu
authors.forename: Changzhi
authors.initials: C
authors.lastname: Wang
authors.forename: Bei
authors.initials: B
authors.lastname: Lin
authors.forename: Qing
authors.initials: Q
authors.lastname: Liu
authors.forename: Yingying
authors.initials: Y
authors.lastname: Hao
authors.forename: Shulan
authors.initials: S
authors.lastname: Zhang
authors.forename: Masao
authors.initials: M
authors.lastname: Iwamori
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015153:Blotting, Western; D000077216:Carcinoma, Ovarian Epithelial; D045744:Cell Line, Tumor; D005260:Female; D005647:Fucosyltransferases / Q000235:genetics / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D007983:Lewis Blood Group Antigens / Q000235:genetics / Q000378:metabolism*; D008875:Middle Aged; D009375:Neoplasms, Glandular and Epithelial / Q000378:metabolism* / Q000473:pathology; D010051:Ovarian Neoplasms / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D017526:Receptor, IGF Type 1 / Q000235:genetics / Q000378:metabolism*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015854:Up-Regulation; D055815:Young Adult; D000097631:Galactoside 2-alpha-L-fucosyltransferase
chemical_list: D005647:Fucosyltransferases; D007983:Lewis Blood Group Antigens; D012333:RNA, Messenger; D017526:Receptor, IGF Type 1; D000097631:Galactoside 2-alpha-L-fucosyltransferase; C094162:Lewis Y antigen
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