title: Receptor for advanced glycation end products (RAGE) and its ligand, amphoterin are overexpressed and associated with prostate cancer development.
abstract: BACKGROUND
  Advanced glycation end products (AGE) are produced with normal aging. Recently, some reports indicated that the interaction between AGE and the cognate receptor (RAGE) has a role in cancer dependent.
  
  
  METHODS
  We investigated RAGE and amphoterin mRNA expression in prostate cancer cell lines (DU145, PC-3, and LNCaP cells), hormone-refractory prostate cancer tissues, and paired untreated primary prostate cancer and normal prostate (including benign prostatic hypertrophy (BPH)) tissues using real-time quantitative PCR. Moreover, to confirm the AGE-RAGE interaction in prostate cancer, DU145 cells stimulated with AGE-bovine serum albumin (AGE-BSA) were examined by in vitro matrigel assay, cell viability assay, MTT assay, reverse transcription-polymerase chain reaction (RT-PCR), and Western blot.
  
  
  RESULTS
  DU145 cells, a hormone-independent prostate cancer cell line, showed the highest RAGE mRNA expression. Amphoterin mRNA was expressed in all three cell lines. In prostate tissues, untreated prostate cancer tissue and hormone-refractory prostate cancer tissue showed higher RAGE and amphoterin mRNA expression than normal prostate tissue. The AGE-RAGE interaction induced the invasion and growth in DU145 cells stimulated with AGE-BSA.
  
  
  CONCLUSIONS
  The AGE-RAGE interaction is important in prostate cancer development, and inhibition of this interaction has potential as a new molecular target for cancer therapy or prevention.
authors.affiliation: Department of Urology, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Ishiguro
authors.forename: Noboru
authors.initials: N
authors.lastname: Nakaigawa
authors.forename: Yasuhide
authors.initials: Y
authors.lastname: Miyoshi
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Fujinami
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Kubota
authors.forename: Hiroji
authors.initials: H
authors.lastname: Uemura
mesh_terms: D015153:Blotting, Western; D045744:Cell Line, Tumor; D002470:Cell Survival; D005562:Formazans; D015972:Gene Expression Regulation, Neoplastic; D017127:Glycation End Products, Advanced / Q000378:metabolism; D024243:HMGB1 Protein / Q000235:genetics*; D006801:Humans; D008024:Ligands; D008297:Male; D009361:Neoplasm Invasiveness; D011470:Prostatic Hyperplasia / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D011471:Prostatic Neoplasms / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology*; D012333:RNA, Messenger / Q000032:analysis; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000235:genetics* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013778:Tetrazolium Salts
chemical_list: D005562:Formazans; D017127:Glycation End Products, Advanced; D024243:HMGB1 Protein; D008024:Ligands; D012333:RNA, Messenger; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; D013778:Tetrazolium Salts; C079782:MTT formazan