Neocarzinostatin-induced Rad51 nuclear focus formation is cell cycle regulated and aberrant in AT cells

Shyng Shiou F. Yuan*, Yuan Kai Yang, Hsiao Wen Chen, Yueh Fang Chung, Hsueh Ling Chang, Jinn Huang Su

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

4 Scopus citations


DNA double-stranded breaks are the most detrimental form of DNA damage and, if not repaired properly, may lead to an accumulation of chromosomal aberrations and eventually tumorigenesis. Proteins of the Rad51/Rad52 epitasis group are crucial for the recombinational repair of DNA double-stranded breaks, whereas the Rad50/NBS1/Mre11 nuclease complex is involved in both the recombinational and the end-joining repair of DNA double-stranded breaks. Herein, we demonstrate that the chemotherapeutic enediyne antibiotic neocarzinostatin induced Rad51, but not NBS1, nuclear focus formation in a cell- cycle-dependent manner. Furthermore, neocarzinostatin-induced Rad51 foci formation revealed a slower kinetic change in AT cells, but not in wild-type or NBS cells. In summary, our results suggest that neocarzinostatin induces Rad51 focus formation through an ATM- and cell-cycle-dependent, but NBS1-independent, pathway.

Original languageEnglish
Pages (from-to)231-236
Number of pages6
JournalToxicology and Applied Pharmacology
Issue number3
StatePublished - 01 11 2003


  • DNA double-stranded breaks
  • End-joining
  • Neocarzinostatin
  • Nuclear focus formation
  • Recombinational repair


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