Exogenous FHIT gene in human gastric cancer cell line MKN45 the impact of migration and invasion.docVIP

 PAGE \* MERGEFORMAT 13 Exogenous FHIT gene in human gastric cancer cell line MKN45 the impact of migration and invasion Of: Liu Fei, Pei-Lin Huang, Huang Zhao-quan, Li Nan, Xu Jiajia, Wu Peng [Abstract] Objective: To explore the fragile histidine triad (FHIT) gene in human gastric cancer MKN 45 cell migration and invasion. Methods: will contain some exogenous FHIT gene eukaryotic expression plasmid pcDNA3.1 FHIT, transfected into FHIT mRNA negative expression in human gastric cancer cell MKN 45, were applied Millicell chamber cell migration assay, Transwell chamber invasion assay transfected MKN 45 cell migration and invasion of the change. Results: Exogenous FHIT gene MKN 45 cells after transfection, MKN 45 cell migration was significantly reduced (P lt;0.05), but no significant changes in cell invasion (Pgt; 0.05). Conclusion: Exogenous FHIT gene transfer induced the migration of MKN 45 cells decreased ability of MKN 45 cells no significant effect on the invasion. [Keywords:] fragile histidine triad; gastric cancer; gene transfer; migration; invasion China is a country of high incidence of gastric cancer, its incidence and mortality rank the forefront of systemic cancer, the incidence rate had an increasing tendency in recent years. Thus, of gastric cancer, the molecular mechanism, so early prevention, early diagnosis and early treatment, to find new therapeutic targets, and effective treatments become a research hotspot. fragile histidine triad (fragile histidine triad, FHIT) gene is equal to 1996, Ohta epithelial cancer cell lines from cloned 3p14.2 region a candidate for suppression oncogene, in a variety of tumor tissues and cell lines that structure and expression of FHIT gene abnormalities have been reported [13]. of the FHIT gene by transfection of exogenous expression of FHIT-negative MKN 45 cells were observed in gastric cancer cell migration , Invasion, for further study of FHIT gene in gastric cancer, the mechanism of the development t