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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Reversal of MRP- mediated multidrug resistance in human lung cancer cells by the antiprogestatin drug RU486.

Multidrug resistance-associated protein ( MRP) and P-glycoprotein (P-gp) are drug efflux pumps conferring multidrug resistance to tumor cells. RU486, an antiprogestatin drug known to inhibit P-gp function, was examined for its effect on MRP activity in MRP-overexpressing lung tumor GLC4/Sb30 cells. In such cells, the antihormone compound was found to increase intracellular accumulation of calcein, a fluorescent compound transported by MRP, in a dose-dependent manner, through inhibition of cellular export of the dye; in contrast, it did not alter calcein levels in parental GLC4 cells. RU486, when used at 10 microM, a concentration close to plasma concentrations achievable in humans, strongly enhanced the sensitivity of GLC4/Sb30 cells towards two known cytotoxic substrates of MRP, the anticancer drug vincristine and the heavy metal salt potassium antimonyl tartrate. Vincristine accumulation levels were moreover up-regulated in RU486-treated GLC4/Sb30 cells. In addition, such cells were demonstrated to display reduced cellular levels of glutathione which is required for MRP-mediated transport of some anticancer drugs. These findings therefore demonstrate that RU486 can down-modulate MRP-mediated drug resistance, in addition to that linked to P-gp, through inhibition of MRP function.[1]


  1. Reversal of MRP-mediated multidrug resistance in human lung cancer cells by the antiprogestatin drug RU486. Payen, L., Delugin, L., Courtois, A., Trinquart, Y., Guillouzo, A., Fardel, O. Biochem. Biophys. Res. Commun. (1999) [Pubmed]
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