Seven of seven different cisplatin-resistant human tumor cell lines sh
owed elevated lipofection activity as compared with their sensitive pa
rent cells, although the degree of enhancement was not quantitatively
correlated with the degree of cisplatin resistance. Enhanced transfect
ion was seen by using the same reporter gene driven by three different
promoter/enhancer sequencer or by using different reporter genes driv
en by the same promoter/enhancer. Cells resistant to actinomycin D, bl
eomycin, and nitrogen mustards were not more transfectable than the se
nsitive parent cells. Although the mechanism of enhanced transfection
in cisplatin-resistant cells is not known, data indicated that enhance
d transcription, multidrug-resistant phenotype, and methallothionein o
verexpression do not play a role.