Inhibition of Human Lung Cancer Cell Growth by the Peroxisome Proliferator-Activated Receptor-γ Agonists through Induction of Apoptosis

Abstract Peroxisome proliferator-activated receptors (PPARs), members of the nuclear hormone receptors superfamily, have an important regulatory role in adipogenesis and inflammation. PPAR-γ ligands induce terminal differentiation and growth inhibition of human breast cancer cells and prostatic cancer cells. In this study, we demonstrated that PPAR-γ, but not PPAR-α, was expressed in human lung cancer cell lines by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis. We also found that the synthetic PPAR-γ agonist thiazolidinedione compounds (troglitazone) and the endogenous PPAR-γ ligand, 15-deoxy-Δ 12,14 -prostaglandin J 2 (15d-PGJ 2 ), inhibited the growth of human lung cancer cells through the induction of apoptosis. However, PPAR-α agonist (bezafibrate) and other prostanoids (PGE 2 , PGF 2α ) did not induce apoptosis. These findings suggest that PPAR-γ may play an important role in the pathogenesis of lung cancer and that PPAR-γ agonist may be useful therapeutic agents in the treatment of human lung cancer.