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Title: Aspirin suppresses components of lymphangiogenesis and lymphatic vessel remodeling by inhibiting the NF-κB/VCAM-1 pathway in human lymphatic endothelial cells
Authors: Prangsaengtong O.
Jantaree P.
Lirdprapamongkol K.
Ngiwsara L.
Svasti J.
Koizumi K.
Keywords: 3 (4 tert butylphenylsulfonyl) 2 propenenitrile
acetylsalicylic acid
immunoglobulin enhancer binding protein
messenger RNA
small interfering RNA
transcription factor RelA
vascular cell adhesion molecule 1
acetylsalicylic acid
immunoglobulin enhancer binding protein
vascular cell adhesion molecule 1
anti-lymphangiogenic effect
cell adhesion
cell migration
concentration (parameters)
controlled study
correlation analysis
drug effect
drug mechanism
endothelium cell
human cell
in vitro study
lymph vessel
priority journal
protein expression
protein phosphorylation
signal transduction
Western blotting
cell motion
cell proliferation
drug effect
endothelium cell
lymph node metastasis
lymph vessel
Cell Movement
Cell Proliferation
Endothelial Cells
Lymphatic Metastasis
Lymphatic Vessels
NF-kappa B
Vascular Cell Adhesion Molecule-1
Issue Date: 2018
Abstract: Lymphangiogenesis is the process of new vessel formation from pre-existing lymphatic vessels. The process mainly involves cell adhesion, migration, and tubule formation of lymphatic endothelial cells. Tumor-induced lymphangiogenesis is an important factor contributing to promotion of tumor growth and cancer metastasis via the lymphatic system. Finding the non-toxic agents that can prevent or inhibit lymphangiogenesis may lead to blocking of lymphatic metastasis. Recently, aspirin, a non-steroidal anti-inflammatory drug (NSAID), has been reported to inhibit in vivo lymphangiogenesis in tumor and incision wound models, but the mechanisms of actions of aspirin on anti-lymphangiogenesis have been less explored. In this study, we aim to explore the mechanism underlying the anti-lymphangiogenic effects of aspirin in primary human dermal lymphatic microvascular endothelial (HMVEC-dLy) cells in vitro. Pretreatment of aspirin at non-toxic dose 0.3 mM significantly suppressed in vitro cord formation, adhesion, and the migration abilities of the HMVEC-dLy cells. Western blotting analysis indicated that aspirin decreased expression of vascular cell adhesion molecule-1 (VCAM-1), at both protein and mRNA levels, and these correlated with the reduction of NF-κB p65 phosphorylation. By using NF-κB inhibitor (BAY-11-7085) and VCAM-1 siRNA, we showed that VCAM-1 expression is downstream of NF-κB activation, and this NF-κB/VCAM-1 signaling pathway controls cord formation, adhesion, and the migration abilities of the HMVEC-dLy cells. In summary, we demonstrate the potential of aspirin as an anti-lymphangiogenic agent, and elucidate its mechanism of action. © 2018, © The Author(s) 2018.
ISSN: 1358863X
Appears in Collections:Scopus 1983-2021

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