Abstract
Degradation of DNA in HeLa-S3 cells mediated by an acidic antitumor protein, neocarzinostatin (NCS), was examined. The concentration of NCS required for induction of DNA degradation was considerably higher than that which caused inhibition of DNA synthesis. Sedimentation analysis of DNA revealed that HeLa-S3 cell DNA first received single-strand nicks within 60 minutes after exposure to the antibiotic, whereas detectable double-strand scissions eventually gave rise to the accumulation of double-stranded DNA fragments of heterogeneous size. When the cells exposed to NCS were transferred to NCS-free medium at early stages of the degradation, the single-strand nicks caused in DNA were repaired by a process which was sensititive to puromycin.
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