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Nucleotide Excision Repair Capacity Is Attenuated in Human Promyelocytic HL60 Cells That Overexpress BCL2¹

Departments of Biological Sciences [Y. L. P. H.] and Pediatrics [L. N.], Stanford University, Stanford, California 94305-5020

We investigated the effect of the BCL2 overexpression on nucleotide excision repair (NER) and DNA replication in UV-irradiated HL60 cells. Forty-eight h after 10 J/m² irradiation, only 4% of the cyclobutane pyrimidine dimers were removed in the BCL2-overexpressing cells, in contrast to 38% removal in control cells. However, the repair of 6-4 pyrimidine pyrimidone photoproducts was not affected by BCL2 overexpression. Eight h after irradiation, DNA replication recovered to 60% of normal in the BCL2-overexpressing cells, whereas little DNA replication recovered in control cells. The antioxidant N-acetyl cysteine also attenuated cyclobutane pyrimidine dimer removal but did not enhance the recovery of DNA replication. Both BCL2-overexpressing and NAC-treated cells were more resistant to UV. Our data suggest that Bcl2 may promote mutagenesis and genomic instability in surviving cells.

¹ This study was supported by Outstanding Investigator Grant CA44349 from the National Cancer Institute (to P. C. H.) and a Cancer Biology Traineeship from Stanford University (to Y. L.). L. N. is the recipient of an Amgen/ASH scholar award.

² To whom requests for reprints should be addressed.

Received 1/22/97. Accepted 3/17/97.

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