Exploration Of Peroxisome Proliferators Activated Receptor Gamma (PPARγ) Ligand Effects To Human Lung Adenocarcinoma A549 Cells

Objective To investigate the expression levels of Peroxisome Proliferators Activated Receptor gamma(PPARγ) in the tissues of non-small cell lung cancer. And the effect of PPARγligand Rosiglitazone (ROZ) on induction of apoptosis in lung adenocarcinoma cell and its possible mechanism.Methods Expression of PPARγwere detected in all 48 specimens of non-small cell lung cancer, 29 specimens of paracancer tissues and 13 specimens with benign pulmonary disease by tissue microarray and immuno- radiometric assay. Human lung adenocarcinoma A549 cell line was cultured in vitro. A549 cell line was treated with various concentration of ROZ, DDP or both. MTT assay, flow cytometry were used to measure the proliferation and apoptosis. The expression of VEGF was detected by immunocyto- chemistry methods after treatment with rosiglitazone.Results (1) PPARγexpressed in NSCLC, lung benign disease and adjacent non-cancer tissues. The expression levels of PPARγin NSCLC were obviously higher than adjacent non-cancer tissues (P<0.05), but no significant correlation was detected in lung benign disease and adjacent non-cancer tissues(P>0.05). (2) The expression levels of PPARγin NSCLC were significantly correlated to cell differentiation and TNM stage, but not correlated with histological classification and lymph node matastasis (P>0.05). (3) Rosiglitazone inhibited the cells proliferation and induced apoptosis in a dose and time-dependent manner, and Rosiglitazone at 1μmol/L significantly increased inhibition growth effect of DDP to A549(P<0.05). (4) Flow cytometry data showed the apoptosis of A549 cells induced by ROZ(1μmol/L) is not significant, but ROZ(1μmol/L) significantly promoted DDP to induce A549 cells apoptosis. (5) VEGF was expressed in A549 cell. Treated with ROZ, A549 cells demonstrated down-regulated expression of VEGF.Conclusion (1) The overexpression of PPARγwere possibly correlated with development, malignancy and matastasia in NSCLC. (2) Rosiglitazone inhibited the cells proliferation by down-regulated expression of VEGF in a dose and time-dependent manner. (3) Rosiglitazone enhanced the sensitization of DDP.