Expression of peroxisome proliferator-activated receptor gamma, E-cadherin and matrix metalloproteinases-2 in gastric carcinoma and lymph node metastases.
- Author:
Qing HE
1
;
Jie CHEN
;
Han-liang LIN
;
Pin-jin HU
;
Min-hu CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Aged; Aged, 80 and over; Cadherins; analysis; Female; Humans; Lymphatic Metastasis; Male; Matrix Metalloproteinase 2; analysis; Middle Aged; PPAR gamma; analysis; Stomach; chemistry; Stomach Neoplasms; chemistry; pathology
- From: Chinese Medical Journal 2007;120(17):1498-1504
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDPeroxisome proliferator activated receptor gamma (PPARgamma) is a ligand-activated transcription factor. Activation of PPARgamma 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 still unknown in gastric carcinoma. The aim of this study was to assess the expression of PPARgamma, E-cadherin, MMP-2 and their correlation in gastric carcinoma and metastases.
METHODSGastric carcinoma tissues and their corresponding lymph nodes with metastases and the adjacent non-tumor tissues were obtained from 54 patients with gastric cancer who underwent gastrectomy. Expression of PPARgamma, E-cadherin and MMP-2 was assessed by immunohistochemical staining.
RESULTSThe nuclear expression level of PPARgamma in neoplastic cells was significantly lower than that in the normal controls (P < 0.001), with the expression of PPARgamma being weaker in primary tumors compared with that in metastases. In all neoplastic cells, E-cadherin was expressed with abnormal patterns (cytoplasm pattern, cytoplasm and membrane pattern or absent), compared with normal cells where E-cadherin was expressed with a normal pattern (membrane pattern). Compared with the normal tissues, the expression level of E-cadherin decreased in primary tumors and further decreased 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 PPARgamma was negatively correlated with MMP-2 expression (P < 0.05). However, there was no correlation between E-cadherin and PPARgamma or MMP-2 expression.
CONCLUSIONSDown-regulation of PPARgamma and E-cadherin and up-regulation of MMP-2 in neoplastic foci might be helpful to gastric carcinogenesis and metastases. An inverse relationship between PPARgamma and MMP-2 in human gastric carcinoma suggests that PPARgamma might modulate MMP-2 expression and affect gastric cancer metastases.