Cell Lung Cancer Cells Maintenance of Elevated Cyclooxygenase-2 in Non-Small Expression Contributes to the α Abnormal Interleukin 10R

Non-small cell lung cancer (NSCLC) cells are known to constitutively overexpress cyclooxygenase (COX)-2. Tumor COX-2-dependent production of PGE2 triggers the synthesis of lymphocyte and macrophage interleukin (IL)-10 that, in turn, is known to potently suppress COX-2 in normal cells. Thus, we investigated the capacity of IL-10 to down-regulate COX-2 expression in NSCLC cells. Western blotting and ELISA analyses revealed that IL-10 did not affect COX-2 expression and subsequent PGE2 production in NSCLC cells. Although normal human bronchial epithelial cells expressed both intracellular and membrane IL-10R , NSCLC cells only expressed intracellular but not cell surface membrane IL-10R . Unresponsiveness of COX-2 to IL-10 is due to the deficiency of IL-10R on the surface of NSCLC cells. Our findings highlight a novel mechanism contributing to maintenance of elevated COX-2 and PGE2 in the lung tumor environment.