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Original ArticleOpen Access
Effects of Selective COX-Inhibitors and Classical NSAIDs on Endothelial Cell Proliferation and Migration Induced by Human Cholangiocarcinoma Cell Culture
Boonmasawai S 
,
Akarasereenont P ,
Techatraisak K ,
Thaworn A ,
Chotewuttakorn S ,
Palo T
,
Akarasereenont P ,
Techatraisak K ,
Thaworn A ,
Chotewuttakorn S ,
Palo T Objective: Experiments were designed to explore cellular mechanisms and effects of NSAIDs on human
umbilical vein endothelial cells (HUVEC) induced by human cholangiocarcinoma (HuCCA).
Material and Method: HUVEC were incubated with HuCCA or HuCCA-conditioned medium (CM) for
various times to determine cell proliferation and migration. Expression of cyclooxygenase (COX) proteins
was measured using immunoblotting technique. VSA (selective COX-1 inhibitor), NS-398 (selective COX-2
inhibitor), and aspirin were used as pharmacological tools to explore signaling mechanisms of HuCCA-CMinduced
endothelial cell functions.
Results: HuCCA could significantly induce proliferation and migration of HUVEC. COX-2, but not COX-1,
was increased. NS-398, but not VSA, could significantly inhibit HuCCA-CM-induced endothelial cell
proliferation. HuCCA-CM-induced endothelial cell proliferations could be also inhibited by aspirin.
Conclusion: These findings suggest that HuCCA-CM-derived substances could induce HUVEC proliferation
through COX-2 signaling mechanism. Classical NSAID and selective COX-2 inhibitors could also inhibit this
step of HUVEC proliferation.
Keywords: Cholangiocarcinoma/ HUVEC/Proliferation/ COX-2/ NSAIDs
umbilical vein endothelial cells (HUVEC) induced by human cholangiocarcinoma (HuCCA).
Material and Method: HUVEC were incubated with HuCCA or HuCCA-conditioned medium (CM) for
various times to determine cell proliferation and migration. Expression of cyclooxygenase (COX) proteins
was measured using immunoblotting technique. VSA (selective COX-1 inhibitor), NS-398 (selective COX-2
inhibitor), and aspirin were used as pharmacological tools to explore signaling mechanisms of HuCCA-CMinduced
endothelial cell functions.
Results: HuCCA could significantly induce proliferation and migration of HUVEC. COX-2, but not COX-1,
was increased. NS-398, but not VSA, could significantly inhibit HuCCA-CM-induced endothelial cell
proliferation. HuCCA-CM-induced endothelial cell proliferations could be also inhibited by aspirin.
Conclusion: These findings suggest that HuCCA-CM-derived substances could induce HUVEC proliferation
through COX-2 signaling mechanism. Classical NSAID and selective COX-2 inhibitors could also inhibit this
step of HUVEC proliferation.
Keywords: Cholangiocarcinoma/ HUVEC/Proliferation/ COX-2/ NSAIDs
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