Clinical Research
Copyright ©The Author(s) 2003. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. May 15, 2003; 9(5): 1094-1097
Published online May 15, 2003. doi: 10.3748/wjg.v9.i5.1094
Bile from a patient with anomalous pancreaticobiliary ductal union promotes the proliferation of human cholangiocarcinoma cells via COX-2 pathway
Gao-Song Wu, Sheng-Quan Zou, Zheng-Ren Liu, Da-Yu Wang
Gao-Song Wu, Sheng-Quan Zou, Zheng-Ren Liu, Da-Yu Wang, Department of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei Province, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr Gao-Song Wu, Department of General Surgery of Tongji Hospital, 1095 Jiefang Road, Wuhan, 430030, Hubei Province, China. wugaosong9172@sina.com
Telephone: +86-27-83662851 Fax: +86-27-83662851
Received: August 24, 2002
Revised: October 1, 2002
Accepted: October 12, 2002
Published online: May 15, 2003
Abstract

AIM: To explore the effects of COX-2 gene in the proliferative activity induced by bile from anomalous pancreaticobiliary ductal union (APBDU) on human cholangiocarcinoma cell line.

METHODS: Bile sample from APBDU and normal bile sample were used for this study. The proliferative effect of bile was measured by methabenzthiazuron (MTT) assay; COX-2 mRNA was examined by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). Cell cycle was analyzed by flow cytometry (FCM), and the PGE2 levels in the supernatant of cultured cholangiocarcinoma cells were quantitated by enzyme-linked immunoabsordent assay (ELISA).

RESULTS: Bile from APBDU can significantly promote the proliferation of human cholangiocarcinoma QBC939 cells compared with normal bile (P = 0.005) and up-regulated remarkably their COX-2 mRNA expression (P = 0.004). The proliferative activity of APBDU bile can be abolished by addition of cyclooxygenase-2 specific inhibitor celecoxib.

CONCLUSION: Bile from APBDU can promote the proliferation of human cholangiocarcinoma QBC939 cells via COX-2 pathway.

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