Effects of COX-2 inhibition on expression of vascular endothelial growth factor and interleukin-8 in lung cancer cells

Abstract

Background: Cyclooxygenase (COX)-2 has been implicated in tumour progression, angiogenesis and metastasis in non-small cell lung cancer (NSCLC). We speculated that inhibition of COX-2 activity might reduce expression of the pro-angiogenic factors vascular endothelial growth factor (VEGF) and interleukin-8 (IL-8) in lung cancer cells.

Proinflammatory Cytokine IL-1β Stimulates IL-8 Synthesis in Mast Cells via a Leukotriene B4 Receptor 2-Linked Pathway, Contributing to Angiogenesis

“…2A), thus excluding the involvement of COX-2-catalized PGs in IL-1b-induced IL-8 synthesis in mast cells. In some cell types such as breast cancer cells and neutrophils, COX-2 has been reported to induce IL-8 synthesis (43,44), whereas in other cell types such as non-small cell lung cancer, IL-8 was produced via a COX-2-independent pathway (45), suggesting that there is a cell typespecific induction pathway of IL-8. Recently, another BLT2 ligand, 12(S)-hydroxyheptadeca-5Z, 8E, 10E-trienoic acid, was identified (46), which is produced by thromboxane synthase from COX-2-metabolized PGH 2 .…”

Tetramethylpyrazine inhibits production of nitric oxide and inducible nitric oxide synthase in lipopolysaccharide-induced N9 microglial cells through blockade of MAPK and PI3K/Akt signaling pathways, and suppression of intracellular reactive oxygen species

“…Upon activation, microglial cells will initiate the secretion of neurotoxic cytokines including tumor necrosis factor-␣ (TNF-␣), interleukin-6 (IL-6), reactive oxygen species (ROS) and nitric products (Ma et al, 2009), which subsequently result in the occurrence of associated neurological diseases. Lipopolysaccharide (LPS), the major portion of outer membrane of gram-negative bacteria, is regarded as a main risk factor responsible for microglial cell activation (Qin et al, 2004;Bi et al, 2005;Zhu et al, 2008). Among LPS-induced inflammation reactions, the over-production of nitric oxide (NO) generated by inducible NO synthase (iNOS) has been paid more attention for its substantial contribution to microglial dysfunction.…”

Chitosan oligosaccharides suppress LPS-induced IL-8 expression in human umbilical vein endothelial cells through blockade of p38 and Akt protein kinases

“…Once activated by extracellular mediators, ECs initiate a variety of inflammatory responses, which ultimately lead to the formation of cardiovascular diseases. Lipopolysaccharide (LPS), the major portion of the outer membrane of gram-negative bacteria, is a strong risk factor for vascular inflammation [2] . In the pathogenesis of infectious diseases, high levels of LPS directly lead to the occurrence of inflammatory responses elicited by ECs, including enhancement of endothelial permeability, secretion of chemokines and recruitment of circulating leukocytes [3] .…”