三氧化二砷诱导人肿瘤细胞凋亡和G2+M期阻滞但引起人永生化宫颈上皮细胞G1期阻滞  

Arsenic Trioxide Induces Human Tumor Cell Apoptosis and G2+M Arrest whereas Causes HPV16 DNA Immortalized Cervical Epithelial Cells G1 Block

作　　者：林晨[1] 邓友平 郑杰[1] 付明[1] 陈洁平 肖培根 吴旻 

机构地区：[1]中国医学科学院

出　　处：《中国医学科学院学报》2000年第2期124-129,共6页Acta Academiae Medicinae Sinicae

摘　　要：目的　研究 As2 O3引起肿瘤细胞凋亡和对细胞周期的影响。方法　采用 DNA凝胶电泳 ,流式细胞仪分析、RT- PCR和 Western免疫印迹等技术检测细胞凋亡的发生。结果　由 As2 O3诱导的人肺腺癌 GL C- 82、胃腺癌 MGC- 80 3和 SGC- 790 1、食管癌 Ec10 9、宫颈癌 He L a细胞凋亡前 ,细胞阻滞在 G2 +M期 ,上述细胞均表现为对c- myc基因的下行调节 ;但在导致永生化人宫颈上皮 HCE16 /3细胞凋亡之前 ,细胞却被阻滞在 G1期 ,对 c- m yc基因表达无影响。结论　 As2 O3引起细胞凋亡与细胞周期阻滞有关 ,在肿瘤细胞和前恶变的 HCE16 /3细胞中阻滞的时期不同 ,这可能与 c-Objective To investigate whether As 2O 3induces tumor cell apoptosis and cell cycle arrest. Methods DNA agarose gel electrophoresis, flowcytometry analysis, RTPCR, and Western blot. Results As 2O 3induced G2+M arrest of tumor cells such as GLC82, MGC803, SGC7901, Eca109 and HeLa cells before inducing apoptosis and decreased cmyc gene expression, whereas caused G1 block of HPV16 DNA immortalized cervical epithelial HCE16/3 cells and did not affect cmyc expression. Conclusions As 2O 3caused apoptosis was related with cell cycle arrest. However, the phase of arrest of tumor cells was different from the pretumor cell HCE16/3 cells, which could be related to the change of cmyc gene expression.

关 键 词：三氧化二砷 细胞凋亡 细胞周期阻滞 肿瘤细胞 

分 类 号：R73-361[医药卫生—肿瘤]