Cisplatin is currently used in tumor chemotherapy to induce the death of 
malignant cells through blockage of DNA replication. It is a commonly used 
chemotherapeutic agent binding mono- or bifunctionally to guanines in DNA. 
Escherichia coli K12 mutant strains deficient in nucleotide excision repair 
(NER) were submitted to increasing concentrations of cisplatin, and the results 
revealed that uvrA and uvrB mutants are sensitive to this agent, while uvrC and 
cho mutants remain as the wild type strain. The time required for both gene 
expression turn-off and return to normal weight DNA in wild-type E. coli was not 
accomplished even after 4 h post-treatment with cisplatin, while the same 
process takes place within 1.5 h after ultraviolet radiation (UV). Besides, a 
heavily damaging action of cisplatin can be seen not only by persistent nicks on 
genomic DNA, but also by NER gene expression exceeding manifold that seen after 
equivalent lethal doses of UV. Moreover, cisplatin caused an increase in uvrB 
gene expression from its putative upstream promoter P3 in an SOS-independent 
manner.