Expression of bax in lung cancer cell apoptosis induced by peroxisome proliferator-activated receptor-γ agonists

Abstract

To discuss the relationship between Bax expression level and lung cancer cell apoptosis induced by peroxisome proliferator-activated receptor-γ (PPAR-γ) agonists. RT-PCR and Western blot analysis were used to detect PPAR-γ expression in the lung cancer cells, and TUNEL was used to detect apoptosis induced by PPAR-γ agonists, while in situ hybridization and immunohistochemistry were used to monitor the changes of Bax mRNA and protein expression levels after apoptosis induced. PPAR-γ expression was detectable in two kinds of lung cancer cells (including Non-small cell lung cancer and small cell lung cancer), and PPAR-γ agonists could inhibit lung cancer growth through inducing apoptosis. The apoptostic rates in control group, 15d-PGJ2 group and ciglitazone group were (1.86±0.49)%, (25.8±2.9)%, and (17.3±1.9)% (P<0.01) respectively; Bax mRNA expression rates in the three groups were (8.75±1.36)%, (66.2±12.86)%, and (29.5±6.5)% (P<0.01) respectively; Bax protein expression rates in the three groups were (9.2±1.45)%, (63±10.4)%, and (34.5±6.0)% (P<0.05) respectively. PPAR-γ is predicted to be a new target in treating lung cancer in the future, and Bax is most likely to work in treating lung cancer apoptosis induced by PPAR-γ agonists as a factor to induced apoptosis.