Background Peroxisome proliferator activated receptor γ(PPARγ)is a ligand-activated transcription factor.Activationof PPARγ has recently been demonstrated to inhibit various tumor cells growth,progression and metastasis.E-cadherin-mediated cell adhesion system is now considered to be an“invasion suppressor system”in cancer tissues.Matrix metalloproteinases-2(MMP-2)is a prerequisite for metastasizing tumor cells.However their correlation is stillunknown in gastric carcinoma.The aim of this study was to assess the expression of PPARγ,E-cadherin,MMP-2 andtheir correlation in gastric carcinoma and metastases.Methods Gastric carcinoma tissues and their corresponding lymph nodes with metastases and the adjacent non-tumortissues were obtained from 54 patients with gastric cancer who underwent gastrectomy.Expression of PPARγ,E-cadherin and MMP-2 was assessed by immunohistochemical staining.Results The nuclear expression level of PPARγ in neoplastic cells was significantly lower than that in the normalcontrols(P<0.001),with the expression of PPARγ being weaker in primary tumors compared with that in metastases.Inall neoplastic cells,E-cadherin was expressed with abnormal patterns(cytoplasm pattern,cytoplasm and membranepattern or absent),compared with normal cells where E-cadherin was expressed with a normal pattern(membranepattern).Compared with the normal tissues,the expression level of E-cadherin decreased in primary tumors and furtherdecreased in metastases(P<0.001).Membrane staining of MMP-2 was detected in the foveolar epithelia of normalgastric mucosa,whereas predominant cytoplasm staining of MMP-2 was found in malignant tissues.The expression ofMMP-2 was stronger in metastatic tissues than in primary tumors.In neoplastic foci the expression of PPARγ wasnegatively correlated with MMP-2 expression(P<0.05).However,there was no correlation between E-cadherin andPPARγ or MMP-2 expression.Conclusions Down-regulation of PPARγ and E-cadherin and up-regulation of MMP-2 in neoplastic foci might behelpful to gastric carcinogenesis and metastases.An inverse relationship between PPARγ and MMP-2 in human gastriccarcinoma suggests that PPARγ might modulate MMP-2 expression and affect gastric cancer metastases.Chin Med J 2007;120(17):1498-1504 Background Peroxisome proliferator activated receptor γ (PPARγ) is a ligand-activated transcription factor. Activation of PPARγ has been demonstrated to inhibit various tumor cell growth, progression and metastasis. E-cadherin-mediated cell adhesion system is now considered to be “ invasion suppressor system ”in cancer tissues. Matrix metalloproteinases-2 (MMP-2) is a prerequisite for metastasizing tumor cells. However their correlation is stillunknown in gastric carcinoma. The aim of this study was to assess the expression of PPARγ, E- cadherin, MMP-2 and the correlation in gastric carcinoma and metastases. Methods Gastric carcinoma tissues and their corresponding lymph nodes with metastases and the adjacent non-tumortissues were obtained from 54 patients with gastric cancer who underwent gastrectomy. Expression of PPARγ, E-cadherin and MMP-2 was assessed by immunohistochemical staining. Results The nuclear expression level of PPARγ in neoplastic cells was significantly lower than th at in the normal controls (P <0.001), with the expression of PPARγ being weaker in primary tumors compared with that in metastases. All neoplastic cells, E-cadherin was expressed with abnormal patterns (cytoplasm pattern, cytoplasm and membrane pattern or absent), compared with with normal cells where E-cadherin was expressed with a normal pattern (membranepattern) .Compared with the normal tissues, the expression level of E-cadherin decreased in primary tumors and furthercreased in metastases (P <0.001) .Membrane staining of MMP-2 was detected in the foveolar epithelia of normal gastric mucosa, whereas predominant cytoplasm staining of MMP-2 was found in malignant tissues. The expression of MMP-2 was stronger in metastatic tissues than in primary tumors. In neoplastic foci the expression of PPAR gamma was negatively correlated with MMP -ow expression (P <0.05) .However, there was no correlation between E-cadherin and PPARγ or MMP-2 expression. Conclusions Down-regulation of PPARγ and E-cadherin and up-regulation of MMP-2 inAnnoplasticity of gastric carcinogenesis and metastases. An inverse relationship between PPARγ and MMP-2 in human gastriccarcinoma suggests that PPARγ might modulate MMP-2 expression and affect gastric cancer metastases. Chin Med J 2007; 120 (17): 1498-1504