Effects of an inhibitor of topoisomerase II, ICRF-193 on the formation of ultraviolet-induced chromosomal aberrations

被引:15
|
作者
Ikushima, T
Shima, Y
Ishii, Y
机构
[1] Kyoto Univ Educ, Div Biol, Fushimi Ku, Kyoto 6120863, Japan
[2] Osaka Univ, Fac Med, Dept Radiat Biol, Osaka 5650871, Japan
关键词
Chinese hamster cell; topoisomerase II inhibitor; ICRF-193; chromosomal aberration; UV;
D O I
10.1016/S0027-5107(98)00092-X
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Treatments of Chinese hamster V79 cells during one cell cycle with a new type of topoisomerase II inhibitor, ICRF-193, which does not accumulate cleavable topoisomerase-DNA complexes induced both chromosome- and chromatid-type aberrations with high frequencies. Furthermore, ICRF-193 synergistically enhanced the yield of UVB-induced chromatid-type aberrations, chromatid exchanges in particular. Treated with ICRF-193 for the last 3 h before harvest, cells showed frequent incidence of chromatid-type aberrations and synergistic enhancement of UVB-induced chromatid-type aberrations, chromatid exchanges in particular. These results suggest that spontaneous and UVB-induced lesions might be ultimately transformed into chromatid-type aberrations by topoisomerase II-dependent checkpoint process(es) in the G(2) phase of the cell cycle. (C) 1998 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:35 / 38
页数:4
相关论文
共 50 条
  • [31] Decreased topoisomerase IIα expression confers increased resistance to ICRF-193 as well as VP-16 in mouse embryonic stem cells
    Kobayashi, M
    Adachi, N
    Aratani, Y
    Kikuchi, A
    Koyama, H
    CANCER LETTERS, 2001, 166 (01) : 71 - 77
  • [32] Ku antigen is required to relieve G2 arrest caused by inhibition of DNA topoisomerase II activity by the bisdioxopiperazine ICRF-193
    Muñoz, P
    Baus, F
    Piette, J
    ONCOGENE, 2001, 20 (16) : 1990 - 1999
  • [33] Characterization of the biological and biochemical activities of F 11782 and the bisdioxopiperazines, ICRF-187 and ICRF-193, two types of topoisomerase II catalytic inhibitors with distinctive mechanisms of action
    van Hille, B
    Etiévant, C
    Barret, JM
    Kruczynski, A
    Hill, BT
    ANTI-CANCER DRUGS, 2000, 11 (10) : 829 - 841
  • [34] INHIBITION OF EUKARYOTIC TOPOISOMERASE-II BY ULTRAVIOLET-INDUCED CYCLOBUTANE PYRIMIDINE DIMERS
    CORBETT, AH
    ZECHIEDRICH, EL
    LLOYD, RS
    OSHEROFF, N
    JOURNAL OF BIOLOGICAL CHEMISTRY, 1991, 266 (29) : 19666 - 19671
  • [35] Differentiation of U-937 promonocytic cells by etoposide and ICRF-193, two antitumour DNA topoisomerase II inhibitors with different mechanisms of action
    Perez, C
    Vilaboa, NE
    GarciaBermejo, L
    deBlas, E
    Creighton, AM
    Aller, P
    JOURNAL OF CELL SCIENCE, 1997, 110 : 337 - 343
  • [36] INHIBITION OF DNA TOPOISOMERASE-II BY ICRF-193 INDUCES POLYPLOIDIZATION BY UNCOUPLING CHROMOSOME DYNAMICS FROM OTHER CELL-CYCLE EVENTS
    ISHIDA, R
    SATO, M
    NARITA, T
    UTSUMI, KR
    NISHIMOTO, T
    MORITA, T
    NAGATA, H
    ANDOH, T
    JOURNAL OF CELL BIOLOGY, 1994, 126 (06): : 1341 - 1351
  • [37] The combination of different types of antitumor topoisomerase II inhibitors, ICRF-193 and VP-16, has synergistic and antagonistic effects on cell survival, depending on treatment schedule
    Ishida, R
    Iwai, M
    Hara, A
    Andoh, T
    ANTICANCER RESEARCH, 1996, 16 (5A) : 2735 - 2740
  • [38] γ-H2AX focus formation in response to ionizing radiation and the topo II targeting drugs, etoposide and ICRF-193
    Sunter, Nicola J.
    Cowell, Ian G.
    Willmore, Elaine
    Durkacz, Barbera W.
    Austin, Caroline A.
    CANCER RESEARCH, 2006, 66 (08)
  • [39] Hypersensitivity of nonhomologous DNA end-joining mutants to VP-16 and ICRF-193 - Implications for the repair of topoisomerase II-mediated DNA damage
    Adachi, N
    Suzuki, H
    Iiizumi, S
    Koyama, H
    JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (38) : 35897 - 35902
  • [40] Hypersensitivity of Ku-deficient cells toward the DNA topoisomerase II inhibitor ICRF-193 suggests a novel role for Ku antigen during the G2 and m phases of the cell cycle
    Muñoz, P
    Zdzienicka, MZ
    Blanchard, JM
    Piette, J
    MOLECULAR AND CELLULAR BIOLOGY, 1998, 18 (10) : 5797 - 5808