To Explore The Molecular Mechanism Of Invasion And Migration Regulated By Cyclooxygenase-2 In Human Gastric Carcinoma Cell In Vitro

Gastric cancer is a malignant tumor with a high incidence, especially in Asian countries, its incidence showed an upgrade trend in recent years. The early clinical symptom of gastric cancer is not typical, and a lot of patients diagnosed with gastric cancer over time and have been part of the transfer of advanced stage with high mortality and poor prognosis. The key of further improve the comprehensive efficacy of gastric cancer is how to early diagnose and monitor recurrence, distant metastasis after surgery. Cyclooxygenase-2 (COX-2) is the key enzyme which catalyzed arachidonic acid into prostaglandin E2 (PGE2). A large number of studies at home and abroad in recent years have showed that COX-2 is over-expression in a variety of solid tumors, which not only involved in the tumorigenesis and tumor development process according to promote cell proliferation, inhibit of apoptosis, but also involved in tumor invasion and metastasis through various mechanisms. To date, the mechanism of COX-2 involved in gastric cancer invasion and metastasis is not clear. In this study, the specific COX-2 inhibitor celecoxib and prostaglandin E2 have been used to intervene in cultured human gastric cancer cell line SGC-7901 in vitro. We explored the effect of COX-2 on the expression of E-cadherin and matrix metalloproteinase2 (MMP-2), as well as the role of COX-2 in gastric cancer and migration and provide valuable indicators of molecular biology for the early diagnosis and treatment of gastric cancer.Aim Celecoxib and PGE2 have been used to intervene in human gastric cancer cell line SGC-7901. We explored the effect of COX-2 on the expression of E-cadherin and MMP-2, as well as the relationship between the expression of COX-2 and E-cadherin, MMP-2, and the mechanism of COX-2 involvement in the tumor cell invasion and migration.Method After celecoxib and PGE2 have been used to intervene in the gastric carcinoma cell line SGC-7901, the real-time quantitative PCR was used to detect the level of COX-2, E-cadherin and MMP-2 mRNA. The combination immunofluorescence and confocal laser scanning microscopy was applied to analyze the expression of E-cadherin protein. Transwell was used to detect the effect of celecoxib and PGE2 on migration and invasive potential of human gastric carcinoma cell.Resultâ‘ In the real-time quantitative PCR, celecoxib significantly inhibited the COX-2 mRNA expression, with a corresponding E-cadherin mRNA expression gradually increased and MMP-2 mRNA expression gradually decreased.â‘¡Application of celecoxib treatment in human gastric cancer cell SGC-7901, the laser confocal fluorescence microscopy detected that the expression of E-cadherin protein significantly increased. On the contrary, the expression of E-cadherin protein decreased significantly after adding PGE2 to the SGC-7901.â‘¢The number of cells in celecoxib treated group through the Transwell chamber was less than the number of cells in the control group showed celecoxib may inhibit SGC-7901 invasion and migration, the number of cells in PGE2 treated group through the Transwell chamber was higher than that of control group showed PGE2 may promote the SGC-7901 invasion and migration.Conclusion Celecoxib may up-regulate the expression of E-cadherin gene and protein, down-regulate the expression of MMP-2 gene and inhibit tumor cell invasion and migration in vitro. PGE2 can down-regulate SGC-7901 cells E-cadherin gene and protein expression, increase MMP-2 gene expression and promote invasion and migration of gastric cancer cell in vitro. Our experiments confirm that COX-2 involved in tumor invasion and migration process by regulating expression of E-cadherin and MMP-2.