Objective: To investigate the relationship between peroxisomeproliferators-activated receptor-gamma (PPAR-γ) and clinical pathology of lung cancer, and to studythe inhibitory effect of PPAR-γ activators on lung canc...Objective: To investigate the relationship between peroxisomeproliferators-activated receptor-gamma (PPAR-γ) and clinical pathology of lung cancer, and to studythe inhibitory effect of PPAR-γ activators on lung cancer growth and the mechanism of inducingapoptosis of lung cancer. Methods: Expression of PPAR-γ in 15 cases of non-cancerous lung tissuesand 64 cases of lung cancer tissues was detected by using immunohistochemistry. The average A valueswere measured by using image analysis. The expression of PPAR-γ in lung cancer cells was detectedby using RT-PCR. After being treated with PPAR-γ activators, apoptosis was detected by using flowcytometry, and meanwhile, the change in caspase-3 activity was detected by caspase-3 kits. Results:Expression levels of PPAR-γ in cancerous tissues were higher than those in non-cancerous lungtissues. In four types of lung cancer, the sequence of PPAR-γ expression from high to low levelswas small-cell lung cancer, squamous carcinom, large-cell lung cancer, adenocarcinoma in turns. Theexpression of PPAR-γ was correlated with differentiation and postoperative TNM staging of lungcancer tissues, but not with lymph node metastasis. PPAR-γ expressed in two lung cancer cell lines,which could induce apoptosis of lung cancer cells after being treated with PPAR-γ activators, andcaspase-3 activity in cells treated with PPAR-γ activators was significantly increased. Conclusion:PPAR-γ is correlated with clinical pathology and apoptosis of lung cancer closely, and activatedPPAR-γ can increase caspase-3 activity to induce cells apoptosis. PPAR-γ will be able to become anew target for therapy of lung cancer in the future.展开更多
文摘Objective: To investigate the relationship between peroxisomeproliferators-activated receptor-gamma (PPAR-γ) and clinical pathology of lung cancer, and to studythe inhibitory effect of PPAR-γ activators on lung cancer growth and the mechanism of inducingapoptosis of lung cancer. Methods: Expression of PPAR-γ in 15 cases of non-cancerous lung tissuesand 64 cases of lung cancer tissues was detected by using immunohistochemistry. The average A valueswere measured by using image analysis. The expression of PPAR-γ in lung cancer cells was detectedby using RT-PCR. After being treated with PPAR-γ activators, apoptosis was detected by using flowcytometry, and meanwhile, the change in caspase-3 activity was detected by caspase-3 kits. Results:Expression levels of PPAR-γ in cancerous tissues were higher than those in non-cancerous lungtissues. In four types of lung cancer, the sequence of PPAR-γ expression from high to low levelswas small-cell lung cancer, squamous carcinom, large-cell lung cancer, adenocarcinoma in turns. Theexpression of PPAR-γ was correlated with differentiation and postoperative TNM staging of lungcancer tissues, but not with lymph node metastasis. PPAR-γ expressed in two lung cancer cell lines,which could induce apoptosis of lung cancer cells after being treated with PPAR-γ activators, andcaspase-3 activity in cells treated with PPAR-γ activators was significantly increased. Conclusion:PPAR-γ is correlated with clinical pathology and apoptosis of lung cancer closely, and activatedPPAR-γ can increase caspase-3 activity to induce cells apoptosis. PPAR-γ will be able to become anew target for therapy of lung cancer in the future.