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

Methods RT-PCR and Western blot analysis were used to detect PPAR-3' expression in the lung cancer cells, and TUNEL was used to detect apoptosis induced by PPAR-3' agonists, while in situ hybridization and immunohistochemistry were used to monitor the changes of Bax mRNA and protein expression levels after apoptosis induced. Results PPAR-3' expression was detectable in two kinds of lung cancer cells (including Non-small cell lung cancer and small cell lung cancer), andl FPAtt-λ/agonists could inhibit lung cancer growth through induci,g apoptosis. The apoptostie rates in cuntroJ group, 15d-PGJ2 group and ciglitazone group were ( 1.86±0.49) %, (25.86± 2.9) %, and ( 17.3 6± 1.9 ) % ( P < 0.01 ) respectively; Bax mRNA expression rates in the three groups were ( 8.756± 1.36) %, (66.26±12.86 ) %, and ( 29.56± 6.5 ) % ( P < 0.01 ) respectively; Bax protein expression rates in the three groups were ( 9.26± 1.45 ) %, ( 63 6± 10.4 ) %, and ( 34.56± 6.0 ) % ( P < 0.05 ) respectively. Conclttsion PPAR-3' 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 hy PPAR-3' agonists as a factor to induce apoptosis.