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目的探讨Burkitt淋巴瘤细胞系Raji中P15INK4B基因甲基化状态,地西他滨对Raji细胞P15INK4B基因去甲基化作用及生长增殖的生物学影响。方法用不同浓度地西他滨作用淋巴瘤细胞株Raji,用台酚蓝拒染法研究药物对Raji细胞生长曲线的影响,采用流式细胞术检测细胞凋亡率,采用聚合酶链反应(RT-PCR)检测P15INK4B表达,用甲基化特异PCR(MSP)方法检测P15INK4B基因的甲基化程度。结果地西他滨对Raji细胞有生长抑制作用,作用后细胞凋亡增加,P15INK4B基因表达增加,地西他滨使其甲基化程度下降。结论在Raji细胞中P15INK4B高度基因甲基化,并且表达下降,地西他滨通过去甲基化抑制淋巴瘤增殖。
Objective To investigate the methylation status of P15INK4B gene in Burkitt lymphoma cell line Raji and the biological effects of decitabine on the demethylation and growth and proliferation of P15INK4B gene in Raji cells. Methods Different concentrations of decitabine were used to effect Raji cell line, and the effect of drug on the growth curve of Raji cells was investigated by trypan blue exclusion assay. The apoptosis rate of Raji cells was detected by flow cytometry. The expression of Raji cells was detected by polymerase chain reaction (RT) -PCR) to detect the expression of P15INK4B. The methylation level of P15INK4B gene was detected by methylation specific PCR (MSP). Results Decitabine could inhibit the growth of Raji cells. After treatment, the apoptosis of Raji cells increased, the expression of P15INK4B increased, and decitabine reduced the methylation of Raji cells. Conclusion The P15INK4B gene is highly methylated in Raji cells and its expression is decreased. Decitabine inhibits the proliferation of lymphoma through demethylation.