Monensin and verapamil do not alter intracellular localisation of daunorubicin in multidrug resistant human KB cells

Cancer Letters
D J WoodJ R Warr

Abstract

The effects of monensin, verapamil and several inhibitors of membrane transport processes on the accumulation of [3H] daunorubicin by human KB-A1 cells have been investigated to determine the role of subcellular vesicular transport in the multidrug resistance phenotype. The Golgi inhibitor, brefeldin A, had no effect on drug accumulation, which suggests that vesicular transport is not a significant factor in drug resistance in these cells. KB-A1 cells were collaterally sensitive to both monensin and verapamil. Both of these compounds reduced drug efflux but did not alter subcellular distribution of daunorubicin, consistent with the view that monensin, like verapamil, acts directly on P-glycoprotein.

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Citations

Sep 7, 2001·Comparative Biochemistry and Physiology. Part A, Molecular & Integrative Physiology·D M Barnes
Jun 11, 2015·Chemical Biology & Drug Design·Michał AntoszczakAdam Huczyński
May 27, 2003·Cytometry. Part a : the Journal of the International Society for Analytical Cytology·Suk W ParkEugene Mechetner
Jul 2, 2019·Chemical Biology & Drug Design·Greta KlejborowskaAdam Huczyński
Jan 22, 2015·Chemical Biology & Drug Design·Iwona SkieraAdam Huczyński

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