Abstract: Objective: To investigate the effect of the exogenous fragile hisdidine triad (FHIT) gene on the proliferation and the apoptosis of gastric cancer cell line MGC-803, and to search for the mechanism of tumor suppression by the FHIT gene. Methods: By the method of liposome transfection, plasmids pRC/CMV-FHIT and pRC/CMV were transfected into the gastric cancer cell line MGC-803 which was absent of FHIT gene expression, and then the transfected cells were screened by G418 and the expression of FHIT was determined by the western blot method. The effect of FHIT on the growth characteristics of gastric cancer cells was observed by MTT, the colony forming test and flow cytometry. Results: Stable FHITexpressing MGC-803 cells were produced, and the proliferation activity and the colony forming capability of MGC-803-FHIT were suppressed, whereas the apoptosis rate of it was increased, and an evident G₀/G₁ phase blockage was also detected. All these differences between MGC-803-FHIT cells and the two control groups of gastric cancer cells had stastical significance. Conclusions: Transfecting the exogenous FHIT gene into gastric cancer cells can suppress the proliferation of tumor cells, and can also induce apoptosis and cell cycle arrest.

Key words: Fragile histidine triad (FHIT) gene, Stomach neoplasms, Gene transfection, Proliferation, Apoptosis