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目的 探讨 FHIT(fragile histidine triad)基因表达在肺癌细胞增殖、凋亡、成瘤性中的作用。方法 应用脂质体转染法构建能高效表达外源性 FHIT基因的 A5 49- FHIT细胞和作为空载体对照的A5 49- vector细胞 ,裸鼠皮下接种构建肺癌移植瘤动物模型 ,应用逆转录 - PCR、Western杂交、免疫组化、流式细胞计数等技术检测外源性 FHIT基因转录、表达及对肺癌细胞株增殖、凋亡、成瘤性等的影响。结果 A5 49- FHIT细胞的生长曲线、克隆形成率、移植瘤体积和重量均显著低于 A5 49- vector和亲本 A5 49细胞 ;A5 49- FHIT细胞凋亡水平显著高于 A5 49- vector和亲本 A5 49细胞 ;与两个对照组相比 ,A5 49- FHIT细胞G0 / G1 比例显著增高。结论 外源性 FHIT表达基因能够显著抑制肺癌细胞增殖和分裂 ,诱导其凋亡 ,抑制其成瘤性 ,提示 FHIT基因在肺癌中具有抑癌基因的功能。
Objective To investigate the role of FHIT (fragile histidine triad) gene in the proliferation, apoptosis and tumorigenesis of lung cancer cells. Methods A549-FHIT cells expressing high level of exogenous FHIT gene and A549-vector cells as empty vector control were constructed by lipofection method. The nude mice were inoculated subcutaneously to establish the lung cancer xenograft model. Reverse transcription- PCR, Western blot, immunohistochemistry, flow cytometry and other techniques to detect exogenous FHIT gene transcription and expression of lung cancer cell proliferation, apoptosis, tumorigenicity and so on. Results The growth curve, colony formation rate and tumor volume and weight of A549-FHIT cells were significantly lower than those of A549-vector and parent A549 cells. The apoptosis of A549-FHIT cells was significantly higher than that of A549-vector and parent A549 cells; Compared with the two control groups, A549-FHIT cells G0 / G1 ratio was significantly increased. Conclusions Exogenous FHIT gene can significantly inhibit the proliferation and division of lung cancer cells, induce apoptosis and inhibit tumorigenicity, suggesting that FHIT gene has the function of tumor suppressor gene in lung cancer.