Publication:
Aspirin suppresses components of lymphangiogenesis and lymphatic vessel remodeling by inhibiting the NF-κB/VCAM-1 pathway in human lymphatic endothelial cells

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Issued Date

2018

Resource Type

Article

File Type

application/pdf

ISSN

1358863X

DOI

10.1177/1358863X18760718

Other identifier(s)

2-s2.0-85045150291

Rights Holder(s)

Scopus

Bibliographic Citation

Vascular Medicine (United Kingdom). Vol 23, No.3 (2018), p.201-211

Suggested Citation

Prangsaengtong O., Jantaree P., Lirdprapamongkol K., Ngiwsara L., Svasti J., Koizumi K. Aspirin suppresses components of lymphangiogenesis and lymphatic vessel remodeling by inhibiting the NF-κB/VCAM-1 pathway in human lymphatic endothelial cells. Vascular Medicine (United Kingdom). Vol 23, No.3 (2018), p.201-211. doi:10.1177/1358863X18760718 Retrieved from: https://hdl.handle.net/20.500.14740/4278

Title

Aspirin suppresses components of lymphangiogenesis and lymphatic vessel remodeling by inhibiting the NF-κB/VCAM-1 pathway in human lymphatic endothelial cells

Author(s)

Prangsaengtong O.
 Jantaree P.
 Lirdprapamongkol K.
 Ngiwsara L.
 Svasti J.
 Koizumi K.

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.

Subject(s)

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
 Article
 Cell adhesion
 Cell migration
 Concentration (parameters)
 Controlled study
 Correlation analysis
 Drug effect
 Drug mechanism
 Endothelium cell
 Human
 Human cell
 In vitro study
 Lymph vessel
 Lymphangiogenesis
 Priority journal
 Protein expression
 Protein phosphorylation
 Signal transduction
 Western blotting
 Cell motion
 Cell proliferation
 Drug effect
 Endothelium cell
 Lymph node metastasis
 Lymph vessel
 Lymphangiogenesis
 Metabolism
 Pathology
 Aspirin
 Cell Movement
 Cell Proliferation
 Endothelial Cells
 Humans
 Lymphangiogenesis
 Lymphatic Metastasis
 Lymphatic Vessels
 NF-kappa B
 Vascular Cell Adhesion Molecule-1

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URI

https://hdl.handle.net/20.500.14740/4278

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Scopus: Year 1983-2021

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