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- W2080394497 abstract "Tumor resistance to oxidative stress prevents the efficacy of cancer therapy based upon a free radical-mediated mechanism.K-rastransformed NIH 3T3 cells (E32-4-2) showed, under oxidative stress, reactive oxygen species (ROS) levels 10-fold lower and lipid peroxide levels 56% lower, compared to their nontransformed counterpart. Since p21rasactivity depends upon farnesylation, we tested the effect of the inhibitors of farnesylation lovastatin and (α-hydroxyfarnesyl) phosphonic acid on susceptibility to oxidative stress in these cells. Preincubation of cells for 24 h with 10 μM lovastatin resulted in a 10-fold increase of ROS levels and a 50% increase of lipid peroxide levels measured under pro-oxidant conditions. Similarly, preincubation of cells with 100 μM (α-hydroxyfarnesyl) phosphonic acid for 24 h enhanced stress-induced levels of either ROS (7.5-fold) or lipid peroxides (33%). The effect of lovastatin and (α-hydroxyfarnesyl) phosphonic acid is specifically due to their ability to inhibit p21rasactivity. In fact, inhibition of p21rasby transfecting E32-4-2 cells with the transdominant negative mutant of H-ras(L61,S186) led, analogously to lovastatin or (α-hydroxyfarnesyl) phosphonic acid treatment, to a strong increase of stress-induced ROS levels. These results suggest that farnesylation inhibitors could be used as an adjuvant therapy to improve the tumoricidal effect of cancer treatment based upon free-radical production inras-dependent tumors." @default.
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- W2080394497 date "1996-12-01" @default.
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- W2080394497 title "Inhibitors of Ras Farnesylation Revert the Increased Resistance to Oxidative Stress in K-rasTransformed NIH 3T3 Cells" @default.
- W2080394497 doi "https://doi.org/10.1006/bbrc.1996.1874" @default.
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