期刊论文

Lei, X.Y.

中文

CANCER COMMUNICATIONS

1000-467X

2002

21

12

1301-1304

10.3969/j.issn.1000-467X.2002.12.005

99M01204G:广东省科技厅科技项目 2001-Z-037-01:广州市科技攻关计划

本校为其他机构

背景与目的:有研究证实,针对bcl-2mRNA翻译起始区和蛋白编码区的2个有效反义作用靶点的反义寡核苷酸能增强HL-60和K562细胞对阿糖胞苷(Ara-C)、柔红霉素、足叶乙甙的敏感性.本研究观察这两个新靶点的反义寡核苷酸对Ara-C诱导原代培养的急性白血病(AL)、慢性淋巴细胞白血病(CLL)细胞凋亡的影响.方法:用细胞记数法观察细胞的生存情况;免疫荧光标记法通过流式细胞仪检测细胞Bcl-2蛋白水平;用姬姆萨染色法观察并用流式细胞仪检测细胞凋亡.结果:靶向bcl-2mRNA翻译起始区与靶向蛋白编码区的两个反义寡核苷酸分别与Ara-C联合作用AL、CLL细胞48h,细胞的活性受到明显的抑制,分别同无关寡核苷酸(NS-ODN)联...

BACKGROUND & OBJECTIVE: The previous study has identified two novel antisense oligonucleotides (AS-ODN) of new target point in the translation initiation and the coding region of bcl-2 mRNA that could increase the sensitivity of HL-60 and K562 cells lines to etoposide, daunorubicin, and araninosyl cytosine (Ara-C). This study was designed to investigate whether the two novel bcl-2 AS-ODNs could increase Ara-C-induced apoptosis of cultured primary acute leukemia (AL) and chronic lymphocytic leukemia (CLL) Cells. METHODS: Cell surviving fraction was determined using the trypan blue dye exclusion...