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目的 研究三联脆组基因 (fragilehistidinetriad ,FHIT)对胰腺癌细胞增殖的影响 ,探讨FHIT基因对胰腺癌增殖的抑癌机制。方法 通过脂质体介导的方法将 pRC/CMVFHIT质粒转染有FHIT全基因丢失的胰腺癌 1990细胞株。用RT PCR及Western blot方法对获得G418抗性细胞进行外源性FHIT基因整合及表达的鉴定。对导入有外源性FHIT基因表达的细胞 (1990 pFHIT)进行细胞生长特征及裸鼠致瘤性分析。经光镜及电镜对 1990pFHIT进行观察 ,并对其进行DNA片段化分析。结果 转染FHIT基因的 1990细胞 ,有外源性FHIT基因的整合及表达 ,其增殖活性明显减弱 ,裸鼠致瘤性明显降低或消失。 1990pFHIT细胞中存在明显的凋亡现象。结论 导入外源性的FHIT基因 ,通过某种途径诱导胰腺癌细胞的凋亡 ,从而抑制肿瘤细胞的恶性增殖。
Objective To study the effect of fragile histidinetriad (FHIT) on the proliferation of pancreatic cancer cells and to explore the mechanism of FHIT gene inhibiting the proliferation of pancreatic cancer. Methods The pRC / CMVFHIT plasmid was transfected into the 1990 pancreatic cancer cell line with full FHIT gene loss by liposome mediated method. The integration and expression of exogenous FHIT gene of G418 resistant cells were confirmed by RT PCR and Western blot. The characteristics of cell growth and tumorigenicity of nude mice were analyzed in cells transfected with exogenous FHIT gene (1990 pFHIT). 1990pFHIT was observed by light microscope and electron microscope, and its DNA fragmentation was analyzed. Results 1990 cells transfected with FHIT gene had exogenous FHIT gene integration and expression, the proliferation activity was significantly weakened, tumorigenicity was significantly reduced or disappeared in nude mice. There was a significant apoptosis phenomenon in 1990pFHIT cells. Conclusion The introduction of exogenous FHIT gene induces the apoptosis of pancreatic cancer cells by some means and thus inhibits the malignant proliferation of tumor cells.