Hypersensitivity in DNA mismatch repair-deficient colon carcinoma cells to DNA polymerase reaction inhibitors
Hypersensitivity in DNA mismatch repair-deficient colon carcinoma cells to DNA polymerase reaction inhibitors
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DOI：
10.1016/j.canlet.2004.07.044
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发表时间：
2005-03-18
期刊：
影响因子：
9.7
通讯作者：
Hemmi, H
中科院分区：
文献类型：
--
作者：
Takahashi, T;Min, Z;Hemmi, H
我们研究了各种DNA复制抑制剂对mmr缺陷和精通结肠癌细胞系的细胞毒性作用。DNA聚合酶（pol）抑制剂包括阿菲迪克林、吉西他滨和羟基脲对hmlh1缺失的HCT116的毒性比对hmlh1精通的HCT116+ch3的毒性更大（1.7 - 2.8倍）。同样，pol抑制剂对hmsh2缺陷LoVo的毒性大于对hmsh2精通的LoVo + ch2的毒性。相比之下，DNA拓扑异构酶I抑制剂，如CPT-11、SN-38和拓扑替康，对mmr熟练细胞的毒性更大。我们的研究结果表明，缺乏ninir的结肠癌细胞对pol反应的抑制剂过敏。2004爱思唯尔爱尔兰有限公司版权所有。
We studied the cytotoxic effects of various DNA replication inhibitors on MMR-deficient and -proficient colon carcinoma cell lines. DNA polymerase (pol) inhibitors including aphidicolin and gemcitabine, and hydroxyurea were more toxic (1.7 to 2.8-fold) to hMLH1-deficient HCT116 than to hMLH1-proficient HCT116+ch3. Similarly, pol inhibitors were more toxic to hMSH2-deficient LoVo than to hMSH2-proficient LoVo + ch2. In contrast, DNA topoisomerase I inhibitors, such as CPT-11, SN-38, and topotecan, were more toxic to MMR-proficient cells. Our results suggest that NINIR-deficient colon carcinoma cells are hypersensitive to inhibitors of the pol reaction. (c) 2004 Elsevier Ireland Ltd. All rights reserved.