Here, we analyzed COX-2 expression in several human lung cancer cell lines and found that COX-2 expression was absent in the H719 and H460 cell lines by a DNA methylation-independent mechanism.
Cyclooxygenase (COX) converts arachidonic acid to prostanoids, and increased expression of its isoform, COX‑2, has been observed in lung cancer tissue.
Here, we report that upregulation of COX-2 can induce overexpression of MRP4 in both A549 non-small-cell lung cancer cell lines and mouse lung cancer models.
A new class of compounds targeting cyclooxygenase 2 (COX-2) together with other different clinically used therapeutic strategies has recently shown a promise for the chemoprevention of several solid tumors including lung cancer.
Here, we show that treatment with TGF-β1 (5 ng/mL) induced downregulation of cyclooxygenase-2 (COX-2), leading to reduced synthesis of prostaglandin E2 (PGE2), in human lung cancer A549 cells.
The aim of this study was to investigate the association of five extensively-studied polymorphisms in PTGS2 (rs689466, rs5275, rs20417) and CYP2E1 (rs2031920, rs6413432) genes with lung cancer risk in a large northeastern Chinese population.
Tubeimoside-1 inhibits proliferation and induces apoptosis by increasing the Bax to Bcl-2 ratio and decreasing COX-2 expression in lung cancer A549 cells.
These results provide evidence that the A allele of Cox-2 intron 6 may be associated with the development of lung cancer and may be a useful marker for early detection and treatment of lung cancer.
The key enzymes in AA metabolism such as cytosolic phospholipase A2 (cPLA(2)) and cyclooxygenase-2 (COX-2) have been implicated in the development and progression of many human cancers, including lung cancer.
Consequently, inhibitors of COX-2 are being studied for their chemopreventative and therapeutic effects in individuals at high risk for lung cancer and patients with established cancers.