Abstract
The expression of H-ras oncogene, it has been shown, induces cisplatin resistance in vitro. Using two types of flat revertants (R1, F32/F33) which lost the transformed phenotypes, we studied the mechanism of the cisplatin resistance. R1 cells, which expressed an activated c-H-ras oncogene, exhibited increased cisplatin resistance. Further, F32/F33 cell lines, which were suppressed the H-ras function by a suppressor mutant of H-ras, restored the cisplatin sensitivity. These results implicate that the cisplatin resistance was directly related to the expression of H-ras and can be circumvented by suppression of the H-ras functions.
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