The human cyclin B1 protein modulates sensitivity of DNA mismatch repair deficient prostate cancer cell lines to alkylating agents

被引：10
|
作者：
Rasmussen, LJ
Rasmussen, M
Lützen, A
Bisgaard, HC
Singh, KK
机构：
[1] Johns Hopkins Oncol Ctr, Johns Hopkins Sch Med, Baltimore, MD 21231 USA
[2] Roskilde Univ, Dept Life Sci & Chem, DK-4000 Roskilde, Denmark
来源：
EXPERIMENTAL CELL RESEARCH | 2000年 / 257卷 / 01期
关键词：
mismatch repair (MMR); cyclin B1; alkylating agents; prostate cancer; DU145; LNCaP;
D O I：
10.1006/excr.2000.4865
中图分类号：
R73 [肿瘤学];
学科分类号：
100214 ;
摘要：
DNA damage caused by alkylating agents results in a G2 checkpoint arrest. DNA mismatch repair (MMR) deficient cells are resistant to killing by alkylating agents and are unable to arrest the cell cycle in G2 phase after alkylation damage. We investigated the response of two MMR-deficient prostate cancer cell lines DU145 and LNCaP to the alkylating agent MNNG. Our studies reveal that DU145 cancer cells are more sensitive to killing by MNNG than LNCaP, Investigation of the underlying reasons for lower resistance revealed that the DU145 cells contain low endogenous levels of cyclin B1. We provide direct evidence that the endogenous level of cyclin B1 modulates the sensitivity of MMR-deficient prostate cancer cells to alkylating agents, (C) 2000 Academic Press.
引用
收藏
页码：127 / 134
页数：8
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