1. Effects of selective COX-inhibitors and classical NSAIDs on endothelial cell proliferation and migration induced by human cholangiocarcinoma cell culture.
- Author
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Boonmasawai S, Akarasereenont P, Techatraisak K, Thaworn A, Chotewuttakorn S, and Palo T
- Subjects
- Analysis of Variance, Blotting, Western, Endothelial Cells drug effects, Endothelium, Vascular cytology, Humans, Neovascularization, Pathologic drug therapy, Staining and Labeling, Tumor Cells, Cultured, Umbilical Veins cytology, Anti-Inflammatory Agents, Non-Steroidal pharmacology, Cell Movement drug effects, Cell Proliferation drug effects, Cholangiocarcinoma drug therapy, Cyclooxygenase Inhibitors pharmacology, Endothelial Cells metabolism
- Abstract
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-CM-induced 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.
- Published
- 2009