| Objective:Gastric cancer is one of the major malignant tumors and its metastasis is the main cause of death of patients with gastric cancer.So that exploring the molecular mechanism of gastric cancer metastasis from different aspects will help us early diagnose and guide clinical for gastric cancer metastasis is of great significance for improving the survival rate and prognosis of patients.This study was aimed at exploring the relationship between circulating tumor cells(CTCs),Epithelial-Mesenchymal Transition,(EMT)and Mesenchymal-Epithelial Transition(MET)in the process of gastric cancer metastasis and provided a new theoretical basis for gastric cancer metastasis and experimental evidence for the targeted treatment of gastric cancer metastasis.Methods:MKN28 cells were inoculated intravenously in twelve Balb/c nude mice after they were cultured and induced by TGF?-1 recombinant protein of final concentration of 10ng/ml for 48 h.After the liver metastasis model of gastric cancer was successfully established,hepatic tissue pathological structure was observed by HE staining.CTCs were isolated from peripheral blood by density gradient centrifugation and confirmed by immunofluorescence staining.At the same time,E-cadherin,N-cadherin,?-catenin and E-cadherin were stained with the first antibody and the second antibody with the corresponding first antibody and the fluorescent labeled second antibody respectively in the gastric cancer cell line MKN28,CTCs and liver metastases and was analyzed and the results were statistically analyzed.Results:Hepatocytes of normal mice G arranged in a cord-like manner and the sinusoids emitted from the central vein and communicated with the central vein,but the central venous wall thickened,inflammatory cells infiltrated and multicellular tumor cells appeared in metastatic mice.After identification,the cells expressed CK19 but CD45,which means we had acquired CTCs.The expression of E-cadherin down-regulated and the expression of N-cadherin,Vimentin,?-catenin up-regulated in CTCs compared with MKN28 cells and the difference was statistically significant(p<0.05).The expression of interstitial molecules N-cadherin?Vimentin??-catenin in hepatic metastases down-regulated compared with CTCs(p<0.05),but the expression of E-cadherin did not change significantly without statistically significant.Conclusions:1.Epithelial-Mesenchymal Transition played an important role in the development of liver metastasis of gastric cancer.2.Circulating tumor cells have characteristic of Epithelial-Mesenchymal Transition.3.Mesenchymal-Epithelial transformation may be involved in the process of CTCs implantation into liver metastases. |
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