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Zapytanie: RAYMOND
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Tytuł oryginału: Influence of G2 arrest on the cytotoxicity of DNA topoismerase inhibitors toward human carcinoma cells with different p53 status.
Autorzy: Bożko Przemysław, Larsen Annette K., Raymond Eric, Składanowski Andrzej
Źródło: Acta Bioch. Pol. 2002: 49 (1) s.109-119, il., bibliogr. 29 poz. - 8 Międzynarodowe Sympozjum pt. Aspekty molekularne chemioterapii Gdańsk 09. 2001
Sygnatura GBL: 303,116

Hasła klasyfikacyjne GBL:
  • toksykologia
  • genetyka
  • farmacja
  • onkologia

    Typ dokumentu:
  • praca związana ze zjazdem
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • in vitro

    Streszczenie angielskie: We here report the influence of the cell cycle abrogator UCN-01 on RKO human colon carcinoma cells differing in p53 status following exposure to two DNA damaging agents, the topoisomerase inhibitors etoposide and camptothecin. Cells were treated with the two drugs at the IC90 concentration for 24 h followed by post-incubation in drug-free medium. RKO cells expressing wild-type, functional p53 arrested the cell cycle progression in both the G1 an G2 phases of the cell cycle whereas teh RKO/E6cells, which lack functional p53, only arrested in the G2 phase. Growth-arrested cells did not resuem proliferetion even after prolonged incubation in drug-free medium (up to 96 h). To evaluate the importance of the cell cycle arrest on cellular survival, a non-toxic dose of UCN-01 (100 nM) was added to the growth-arrested cells. The addition of UCN-01 was accompanied by mitotic entry as revealed by the appearance of condensed chromatin and the MPM-2 phosphoepitope, which is charactieristic for mitotic cells, G2 exit and mitotic transit was accompanied by a rapid activation of caspase-4 and apoptotic cell death. The influence of UCN-01 on the long-term cytotoxic effects of the two drugs was also determined. Unexpectedly, abrogation of the G2 arrest had no influence on the overall cytotoxicity of either drug. In contrast, addition of UCN-01 to cisplatin-treated RKO and RKO/E6 cells greatly increased the cytotoxic effects of the alkylating agent. These results strongly suggest that even prolonged cell cycle arrest in the G2 phase of the cell cycle is not necessarily coupled to efficient DNA repair and enhanced cellular survival as generally believed.

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