外源性FHIT基因对人胃癌细胞株MGC-803增殖与凋亡的影响

目的：研究三联脆性组氨酸基因（fragile histidine triad，FHIT）对胃癌细胞株MGC 803增殖与凋亡作用的影响，并探讨FHIT基因的抑癌机制。方法：通过脂质体介导把质粒pRC/CMV-FHIT及pRC/CMV转染到有FHIT基因表达缺失的胃癌细胞株MGC-803，用G418对转染后细胞进行筛选，用Western blot对获得G418抗性的细胞进行FHIT基因表达的鉴定。用MTT法、克隆形成试验及流式细胞术观察转染前后细胞生长特性的变化。 结果：转染FHIT基因的MGC-803细胞有外源性FHIT基因的表达，其增殖活性减弱、克隆形成能力降低、凋亡率增加、生长周期出现明显的G₀/G₁期阻滞,且与对照组差异均有统计学意义。结论：向胃癌细胞中导入外源性FHIT基因可以抑制肿瘤细胞增殖，诱导细胞凋亡并引起细胞生长周期阻滞。

Effect of the exogenous fragile histidine triad (FHIT) gene on proliferation and apoptosis of gastric cancer cell line MGC-803

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.