XPF的失活使癌细胞对吉西他滨敏感。

IF 1.3 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Nucleic Acids Pub Date : 2019-03-03 eCollection Date: 2019-01-01 DOI:10.1155/2019/6357609
Joseph W George, Mika Bessho, Tadayoshi Bessho
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引用次数: 2

摘要

吉西他滨(2′,2′-二氟脱氧胞苷;dFdC)是脱氧胞苷类似物,主要用于治疗胰腺癌。吉西他滨的细胞毒性是由于抑制DNA复制。然而,去除合并dFdC的机制在很大程度上是未知的。在本报告中,我们发现核苷酸切除修复蛋白XPF- ercc1参与了吉西他滨诱导的DNA损伤的修复,XPF的失活使细胞对吉西他滨敏感。进一步分析发现,XPF-ERCC1与apurinic/ ap嘧啶内切酶(APE)共同作用于吉西他滨诱导的DNA损伤修复。我们的结果证明了评估DNA修复活性在吉西他滨治疗中的重要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Inactivation of XPF Sensitizes Cancer Cells to Gemcitabine.

Gemcitabine (2', 2'-difluorodeoxycytidine; dFdC) is a deoxycytidine analog and is used primarily against pancreatic cancer. The cytotoxicity of gemcitabine is due to the inhibition of DNA replication. However, a mechanism of removal of the incorporated dFdC is largely unknown. In this report, we discovered that nucleotide excision repair protein XPF-ERCC1 participates in the repair of gemcitabine-induced DNA damage and inactivation of XPF sensitizes cells to gemcitabine. Further analysis identified that XPF-ERCC1 functions together with apurinic/apyrimidinic endonuclease (APE) in the repair of gemcitabine-induced DNA damage. Our results demonstrate the importance of the evaluation of DNA repair activities in gemcitabine treatment.

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来源期刊
Journal of Nucleic Acids
Journal of Nucleic Acids BIOCHEMISTRY & MOLECULAR BIOLOGY-
CiteScore
3.10
自引率
21.70%
发文量
5
审稿时长
12 weeks
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