Published online Jan 15, 2003. doi: 10.3748/wjg.v9.i1.184
Revised: July 23, 2002
Accepted: July 31, 2002
Published online: January 15, 2003
AIM: 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 PGE2 levels in the supernatant of cultured cholangiocarcinoma cells were quantitated by enzyme-linked immunoabsordent 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 µM). 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).
CONCLUSION: Bile from congenital choledochal cyst patients can promote the proliferation of human cholangiocarcinoma QBC939 cells via COX-2 and PGE2 pathway.