Cyclooxygenase‐2 inhibitor NS‐398 suppresses cell growth and constitutive production of granulocyte‐colony stimulating factor and granulocyte macrophage‐colony stimulating factor in lung cancer cells

Abstract

We previously established two lung cancer cell lines, OKa-C-1 and MI-4, which constitutively produce abundant granulocyte-colony stimulating factor (G-CSF) and granulocyte macrophage-colony stimulating factor (GM-CSF). Inflammatory cytokines, tumor necrosis factor-alpha (TNF-α α α α) and interleukin ( ccasionally, leukocytosis is observed in patients with several cell types of carcinoma with an aggressive clinical course.

Granulocyte colony stimulating factor alters the phenotype of neuroblastoma cells: implications for disease-free survival of high-risk patients

“…Our results indicate that neuroblastoma cell lines do express the mRNA for the GCSF-receptor (Figure 1) and respond to exogenous GCSF stimulation. The propensity for tumor cells to respond to growth factors is readily observed in several types of cancer [9][10][11][12][13]. This documented response to growth factors, coupled with the observation that neuronal progenitor cells utilize GCSF as a growth and development factor in normal development [15] suggest that these cells either never lose GCSF receptor expression, or reclaim expression as part of functional changes during mutagenesis or oncogenesis [16].…”

“…Specifically, GCSF has been associated with tumor progression, increased invasiveness and poorer prognosis in tumors such as head and neck squamous cell carcinoma [9], non-small cell lung cancer [10,11], bladder [12] and prostate cancer [13]. The reported association between GCSF, GCSF receptors and other tumors led us to question whether GCSF has an effect on neuroblastoma tumor growth.…”

The COX-2 Selective Inhibitor-Independent COX-2 Effect on Colon Carcinoma Cells is Associated with the Delta1/Notch1 Pathway

“…Recent have identified a series of new molecular targets for NSAIDs that are mainly involved in signaling pathways; these include 15-lipoxygenase-1 [6], extracellular signalregulated kinase 1/2 signaling [7], nuclear factor kappaB (NF-_B) [8] and the Akt/PKB kinases [9].…”

Effects of an ophthalmic formulation of meloxicam on COX-2 expression, PGE2 release, and cytokine expression in a model of acute ocular inflammation

“…Increased COX-2 activity upregulates several components of the signalling cascade of activation of some cytokines and is intimately related with the inflammatory process 4. IL-1β secretion induces PGE 2 production through activation of COX-2 and cJun-N-terminal kinase 5.…”