摘要
目的 :通过分析人支气管上皮细胞BEP2D和其α粒子诱发的癌变细胞系BERP35T1和BERP35T4的纺锤体检测点功能 ,探讨纺锤体检测机制变化在辐射致癌中的作用。 方法 :用噻氨酯哒唑药物破坏细胞的微管结构 ,导致纺锤体形成受阻 ,在光学显微镜下计数有丝分裂细胞。 结果 :本实验观察的辐射诱发癌变细胞系中有的染色体数目相对稳定 ,有的不稳定 ,其中表现为多倍体细胞比例增高。通过分析纺锤体检测点机制 ,发现染色体数目异常(多倍体)比例高的癌变细胞BERP35T4(40 %)在噻氨酯哒唑药物作用后12～24h,有丝分裂指数(MI)明显低于亲本BEP2D细胞和另一癌变细胞系BERP35T1 ,后二者细胞的多倍体率较低(5 %)。 结论
Purpose: To analyze the spindle checkpoint function of BEP2D cells ant its malignant transformed cell lines induced by α_particles. Methods: Nocodazole, the inhibitor of spindle construction, was used to destroy the microtubule and initiate the spindle checkpoint mechanism to arrest the cells in the phase of mitosis, and mitotic index(MI) was counted under microscope. Results: BERP35T4 is a αparticles_induced transformed cell line with chromosome instability manifesting increased polyploids. After the treatment with nocodazole for 12～24 h, the mitotic index of BERP35T4 was significantly lower than that of the parental BEP2D cells and BERP35T1, another transformed cell line with relatively stable cytogenetic state. Conclusion: The spindle_checkpoint mechanism was deficient in BERP35T4 cells, and it could be related to the chromosome instability and the transformation of this cell line initiated by α particles exposure.
出处
《癌变·畸变·突变》
CAS
CSCD
2003年第2期65-67,共3页
Carcinogenesis,Teratogenesis & Mutagenesis
基金
国家高技术研究发展计划(863计划
No.2001AA221271)
国家自然科学基金(No.30270423)
"十五"军队医学杰出中青年基金(No.01J006)
