Jongkonnee ThanasaiTemduang LimpaiboonPatcharee JearanaikoonBanchob SripaChawalit PairojkulSrisurang Tantimavanich,Masanao Miwa2011-06-302017-06-202011-06-302017-06-202011-06-302010World J Gastroenterol. Vol.16, No.13 (2010), 1631-16381007-93271007-9327 (print)https://repository.li.mahidol.ac.th/handle/20.500.14594/2073AIM: To evaluate the role of thymidine phosphorylase (TP) in cholangiocarcinoma using small interfering RNA (siRNA). METHODS: A human cholangiocarcinoma-derived cell line KKU-M139, which has a naturally high level of endogenous TP, had TP expression transiently knocked down using siRNA. Cell growth, migration, in vitro angiogenesis, apoptosis, and cytotoxicity were assayed in TP knockdown and wild-type cell lines. RESULTS: TP mRNA and protein expression were decreased by 87.1% ± 0.49% and 72.5% ± 3.2%, respectively, compared with control cells. Inhibition of TP significantly decreased migration of KKU-M139, and suppressed migration and tube formation of human umbilical vein endothelial cells. siRNA also reduced the ability of TP to resist hypoxia-induced apoptosis, while suppression of TP reduced the sensitivity of KKU-M139 to 5-fluorouracil. CONCLUSION: Inhibition of TP may be beneficial in decreasing angiogenesis-dependent growth and migration of cholangiocarcinoma but may diminish the response to 5-fluorouracil chemotherapy.engLiver flukeCholangiocarcinomaThymidine phosphorylase5-fluorouracilTumor aggressivenessCell migrationsiRNAOpen Access articleArticledoi:10.3748/wjg.v16.i13.1631