Cyclooxygenase-2 is associated with malignant phenotypes in human lung cancer

The objective of the present study was to investigate whether cyclooxygenase-2 (COX-2) is associated with malignancy, and to investigate its molecular mechanisms in human lung cancer tumor malignancy. The present study used RNA interference (RNAi) methodology and celecoxib, a COX-2 inhibitor, to investigate the effect of COX‑2 knockdown on the proliferation and invasion abilities of lung cancer cells and the molecular mechanisms involved. Human lung adenocarcinoma A549‑si10 and LTEP‑A2 cells transfected with a specific small interfering RNA (A549‑si10 and LTEP‑A2‑si10, respectively) grew more slowly compared with parental cell lines and cells transfected with pU6. The colony formation of A549‑si10 and LTEP‑A2‑si10 cells was also reduced. In addition, A549‑si10 and LTEP‑A2‑si10 cells were characterized by decreased metastatic and invasive abilities. The proliferation and invasive potential of parental A549 and LTEP‑A2 cells was inhibited following treatment with celecoxib. In vivo, a COX‑2 knockdown resulted in a decrease of proliferation and reduction of vascular endothelial growth factor (VEGF), matrix metalloproteinase‑2 (MMP‑2) and endothelial growth factor receptor (EGFR) expression in A549 xenografts. In conclusion, the present study revealed that COX‑2 plays a extremely important role in tumor growth, infiltration and metastasis via the regulation of VEGF, MMP‑2 and EGRF expression. Therefore, COX‑2 is a potential therapeutic target for lung cancer.