Proliferative activity of bile from congenital choledochal cyst patients.
World J Gastroenterol
; 9(1): 184-7, 2003 Jan.
Article
en En
| MEDLINE
| ID: mdl-12508379
ABSTRACT
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 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).CONCLUSION:
Bile from congenital choledochal cyst patients can promote the proliferation of human cholangiocarcinoma QBC939 cells via COX-2 and PGE(2) pathway.
Texto completo:
1
Banco de datos:
MEDLINE
Asunto principal:
Bilis
/
Carcinógenos
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Quiste del Colédoco
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División Celular
Límite:
Adolescent
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Adult
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Animals
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Child
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Child, preschool
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Revista:
World J Gastroenterol
Asunto de la revista:
GASTROENTEROLOGIA
Año:
2003
Tipo del documento:
Article
País de afiliación:
China