bcl-x_s促进三氧化二砷诱导鼻咽癌细胞凋亡的研究

目的　利用促进凋亡基因bcl-xs 降低肿瘤细胞凋亡阈值 ,增强三氧化二砷诱导的鼻咽癌细胞凋亡 ,以探索提高鼻咽癌化疗敏感性的新途径。方法　将含有人bcl -xs 基因的重组真核表达质粒导入人鼻咽癌低分化上皮细胞株 (CNE - 2Z) ,以不含有bcl-xs 基因的质粒转染CNE - 2Z作为对照细胞。用三氧化二砷处理两组细胞后 ,台盼蓝计数法求得各自的IC50 ,流式细胞仪检测凋亡细胞百分比。结果　导入bcl-xs 的细胞与对照细胞相比 ,其对三氧化二砷的IC50 值明显降低 ,流式细胞仪及荧光染色检测结果表明其凋亡细胞百分比明显高于对照细胞。结论　bcl-xs 能显著提高鼻咽癌CNE - 2Z细胞株对三氧化二砷诱导凋亡的敏感性

Bcl-x_s promotes arsenic trioxide-induced apoptosis in nasopharyngeal carcinoma cells

Objective To decrease the threshold of apoptosis in human nasopharyngeal carcinoma cells in order to explore a new strategy to enhance the sensitivity of chemotherapy by apoptosis-promoting gene bcl-x s. Methods Bcl-x s gene-bearing mammalian expression vector was transfected into CNE-2Z cells. Cells with no transfected bcl-x s gene were taken as controls. After the treatment with arsenic trioxide, IC 50 was calculated using trypan blue exclusion. Apoptotic cells were detected with flow cytometry. Results The IC 50 of cells expressing transfected bcl-x s, treated with arsenic trioxide, significantly decreased compared with that of the controls. The results of flow cytometry analysis showed a significant increase of apoptotic cells in CNE-2Zx s as compared with the controls after treating with the same amount of arsenic trioxide. Conclusion Exogenous bcl-x s expression can enhance the sensitivity of CNE-2Z to arsenic trioxide-induced apoptosis.