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作 者:黄洪晖[1] 朱坚轶[1] 顾春红[1] 王海嵘[1] 滕晔[1] 陈芳源[1]
机构地区:[1]上海第二医科大学仁济医院血液科上海血液学研究所,上海200001
出 处:《上海第二医科大学学报》2005年第5期437-439,458,共4页Acta Universitatis Medicinalis Secondae Shanghai
基 金:国家自然科学基金(30271660)资助项目.
摘 要:目的探讨硫化砷诱导急性早幼粒细胞白血病(APL)细胞凋亡的分子机制。方法应用基因表达谱芯片、RTPCR技术,检测硫化砷作用前后NB4细胞、APL原代细胞PNAS-2基因表达的变化。结果基因表达谱芯片杂交显示,硫化砷作用于NB4细胞后,PNAS-2基因表达下调;RTPCR结果发现,NB4细胞在硫化砷作用后PNAS-2表达有明显下调,并呈时间依赖性;APL原代细胞经硫化砷作用后,PNAS-2表达也呈下降趋势。结论硫化砷能够下调PNAS2基因在NB4细胞株和APL原代细胞中的表达,推测PNAS-2基因可能是硫化砷治疗APL的靶基因之一。Objective To study the molecular biological mechanisms of cell apoptosis in acute promyelocytic leukemia(APL) cells induced by arsenic sulfide. Methods The techniques of gene chips and RT-PCR were used to investigate the altered expression of PNAS-2 gene in arsenic sulfide treated NB4 cells and leukemia cells from APL patients. Results The study of gene chips revealed that in arsenic sulfide treated NB4 cells the expression of PNAS-2 gene was down regulated. The RT-PCR experiment showed that in NB4 cells PNAS-2 transcripts were in lower amounts after treatment with arsenic sulfide, and the effect was time-dependent; the same results could be found in leukemia cells from APL patients. Conclusion Arsenic sulfide can down regulate the expression of PNAS-2 gene in NB4 cells and leukemia cells from APL patients. It suggested the PNAS-2 gene might be one of the target genes of arsenic sulfide anti-APL effects.
关 键 词:急性早幼粒白血病细胞 急性早幼粒细胞白血病 基因表达谱芯片 硫化砷作用 RT-PCR技术 原代细胞 NB4细胞株 时间依赖性 APL 分子机制 细胞凋亡 方法应用 表达下调 下降趋势 砷诱导 靶基因
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