Abstract
BackgroundIt has been demonstrated that urokinase-type plasminogen activator (uPA) is involved in tumor cell metastasis by degrading the extracellular matrix. However, there is little direct evidence of clinical uPA system expression in peritoneal metastatic tissues of gastric cancer. The objective of this study was to investigate uPA system expression in peritoneal tissues of peritoneal and nonperitoneal metastasis patients, and to explore the diagnostic value of the uPA system.MethodsExpressions of uPA, uPAR, and PAI-1 were measured by semi-quantitative RT-PCR and ELISA. uPA activity was detected using a uPA activity kit.ResultsThere was no significant difference in uPA, uPAR, and PAI-1 expression in two types of peritoneal tissue in seven patients with peritoneal metastasis. However, uPA, uPAR, and PAI-1 expressions in peritoneal metastatic lesions were significantly higher than those in normal peritoneal tissues of 24 nonperitoneal metastasis patients (P <0.05). Moreover, no statistical discrepancy of uPA activity was observed in various different tissues.ConclusionsThe expression of the uPA system positively correlates with peritoneal metastasis of gastric cancer. This expression difference in peritoneal or nonperitoneal metastasis patients may provide a reference for diagnosis of peritoneal metastasis.
Highlights
It has been demonstrated that urokinase-type plasminogen activator is involved in tumor cell metastasis by degrading the extracellular matrix
Semi-quantitative Reverse transcriptase (RT)-Polymerase chain reaction (PCR) analysis of carcinoembryonic antigen (CEA), urokinase-type plasminogen activator (uPA), uPA receptor (uPAR), and PAI-1 mRNA expression CEA is an important marker for gastroenteric tumors
Thereby, we used a high sensibility nested Reverse transcriptase polymerase chain reaction (RT-PCR) method to detect the expression of CEA in gastric cancer tissues with or without peritoneal metastasis
Summary
It has been demonstrated that urokinase-type plasminogen activator (uPA) is involved in tumor cell metastasis by degrading the extracellular matrix. There is little direct evidence of clinical uPA system expression in peritoneal metastatic tissues of gastric cancer. It has been observed that the uPA system is well correlated with gastric cancers, by measuring the expression level of uPA, uPAR, and PAI-1 in gastric cancer and normal mucosal tissue and analyzing their correlation with various clinical pathological characteristics. Plebani et al [10] determined uPAR, uPA, and PAI-1 levels using ELISA in gastric cancer and normal samples from 20 patients with gastric cancer undergoing surgery. The expressions of uPA, uPAR, and PAI-1 are significantly correlated with various clinicopathological factors: tumor size, depth of tumor invasion, differentiation, lymph node metastasis [12,13,14,15], and peritoneum metastasis [16,17]
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