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UCN-01 (7-hydroxystaurosporine) inhibits DNA repair and increases cytotoxicity in normal lymphocytes and chronic lymphocytic leukemia lymphocytes.
http://hdl.handle.net/10098/1124
http://hdl.handle.net/10098/1124bf115e08-b208-454a-a743-b1f596e84041
名前 / ファイル | ライセンス | アクション |
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yamauchi_UCN.pdf (237.2 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2007-09-19 | |||||
タイトル | ||||||
タイトル | UCN-01 (7-hydroxystaurosporine) inhibits DNA repair and increases cytotoxicity in normal lymphocytes and chronic lymphocytic leukemia lymphocytes. | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | DNA damage | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | nucleotide excision repair | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | cyclophosphamide | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | chronic lymphocytic leukemia | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | UCN-01 | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_1843 | |||||
資源タイプ | other | |||||
著者 |
Yamauchi, Takahiro
× Yamauchi, Takahiro× Keating, Michael J.× Plunkett, William |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Elevated DNA repair processes represent resistance mechanisms to the treatment of malignancies with alkylating agents. Recently, the cell cycle checkpoint abrogator, UCN-01, was reported to inhibit nucleotide excision repair in cell-free systems. We hypothesized that if UCN-01 was combined with DNA-damaging agents, UCN-01 might inhibit the damage repair processes, thereby enhancing cytotoxicity in quiescent cells. Here, we investigated the effect of UCN-01 on DNA repair and viability of quiescent normal lymphocytes and chronic lymphocytic leukemia lymphocytes treated with UV or the cyclophosphamide prodrug 4-hydroperoxycyclophosphamide (4-HC). DNA damage repair kinetics were determined as DNA single strand breaks by the alkaline single cell gel electrophoresis (comet) assay and by [3H]thymidine incorporation. Pretreatment with UCN-01 inhibited DNA repair initiated by UV or 4-HC in normal lymphocytes as well as chronic lymphocytic leukemia lymphocytes in a concentration-dependent manner at clinically relevant levels (50-300 nM). This inhibition was demonstrated by the decreases in incision capability, DNA resynthesis, and in rejoining, suggesting that UCN-01 inhibits the multiple sites of the repair processes. The higher UCN-01 concentration (300 nM) maximized the inhibitory effects and enhanced the UV- or 4-HC-induced cytotoxicity, as determined by annexin V binding or Hoechst 33342 staining. This enhancement was not obtained by the lower concentrations that incompletely inhibited the repair, suggesting the close association between the inhibition of the repair and the enhancement of the cytotoxicity. Our findings suggest that UCN-01 may be a good candidate for combination strategies of cancer treatment. | |||||
書誌情報 |
Molecular cancer therapeutics 巻 1, 号 4, p. 287-294, 発行日 2002-02 |
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出版者 | ||||||
出版者 | American Association for Cancer Research, Inc., | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 15357163 | |||||
書誌レコードID | ||||||
識別子タイプ | NCID | |||||
関連識別子 | TD00006284 |