Nucleotide excision repair capacity is attenuated in human promyelocytic HL60 cells that overexpress BCL2.

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.