Gao-Song Wu1, Sheng-Quan Zou, Xian-Wen Luo, Jian-Hong Wu, Zheng-Ren Liu. 1. Department of General Surgery, Tongji Hospital, Tongji Medical College Huazhong University of Science and Technology, Wuhan, 430030, Hubei Province, China. wugaosong9172@sina.com
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.
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 humancholangiocarcinoma 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 humancholangiocarcinoma QBC939 cells via COX-2 and PGE(2) pathway.
Authors: L Li; A Yamataka; W Yian-Xia; W Da-Yong; O Segawa; G J Lane; W Kun; Z Jin-Zhe; T Miyano Journal: J Pediatr Surg Date: 2001-11 Impact factor: 2.545
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