title: Proliferative activity of bile from congenital choledochal cyst patients.
abstract: OBJECTIVE
  To explore the potential carcinogenicity of bile from congenital choledochal cyst (CCC) patients and the mechanism of the carcinogenesis in congenital choledochal cyst patients.
  
  
  METHODS
  20 bile samples from congenital choledochal cyst patients and 10 normal control bile samples were used for this study. The proliferative effect of bile was measured by using Methabenzthiazuron (MTT) assay; Cell cycle and apoptosis were analyzed by using flow cytometry (FCM), and the PGE(2) levels in the supernatant of cultured cholangiocarcinoma cells were quantitated by enzyme-linked immunoabsorbent assay (ELISA).
  
  
  RESULTS
  CCC bile could significantly promote the proliferation of human cholangiocarcinoma QBC939 cells compared with normal bile (P=0.001) and negative control group (P=0.002), and the proliferative effect of CCC bile could be abolished by addition of cyclooxygenase-2 specific inhibitor celecoxib (20 microM). The QBC939 cells proliferative index was increased significantly after treated with 1 % bile from CCC patient (P=0.008) for 24 h, the percentage of S phase (29.48+/-3.27)% was increased remarkably (P<0.001) compared with normal bile (11.72+/-2.70) %, and the percentage of G0/G1 phase (54.19+/-9.46) % was decreased remarkably (P=0.042) compared with normal bile (69.16+/-10.88) %, however, bile from CCC patient had no significant influence on apoptosis of QBC939 cells (P=0.719).
  
  
  CONCLUSIONS
  Bile from congenital choledochal cyst patients can promote the proliferation of human cholangiocarcinoma QBC939 cells via COX-2 and PGE(2) pathway.
authors.affiliation: Department of General Surgery, Tongji Hospital, Tongji Medical College Huazhong University of Science and Technology, Wuhan, 430030, Hubei Province, China. wugaosong9172@sina.com
authors.forename: Gao-Song
authors.initials: GS
authors.lastname: Wu
authors.forename: Sheng-Quan
authors.initials: SQ
authors.lastname: Zou
authors.forename: Xian-Wen
authors.initials: XW
authors.lastname: Luo
authors.forename: Jian-Hong
authors.initials: JH
authors.lastname: Wu
authors.forename: Zheng-Ren
authors.initials: ZR
authors.lastname: Liu
mesh_terms: D000293:Adolescent; D000328:Adult; D000818:Animals; D017209:Apoptosis; D001646:Bile / Q000378:metabolism*; D002273:Carcinogens; D000068579:Celecoxib; D002453:Cell Cycle; D002455:Cell Division; D002648:Child; D002675:Child, Preschool; D015529:Choledochal Cyst / Q000378:metabolism*; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007527:Isoenzymes / Q000378:metabolism; D008297:Male; D008565:Membrane Proteins; D008875:Middle Aged; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D011720:Pyrazoles; D013449:Sulfonamides / Q000378:metabolism; D014407:Tumor Cells, Cultured
chemical_list: D002273:Carcinogens; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007527:Isoenzymes; D008565:Membrane Proteins; D011720:Pyrazoles; D013449:Sulfonamides; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D000068579:Celecoxib; D015232:Dinoprostone