alexa Modulation of multidrug resistance by artemisinin, artesunate and dihydroartemisinin in K562 adr and GLC4 adr resistant cell lines.
Immunology

Immunology

International Journal of Inflammation, Cancer and Integrative Therapy

Author(s): Reungpatthanaphong P, Mankhetkorn S, Reungpatthanaphong P, Mankhetkorn S

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Abstract Overcoming MDR (multidrug resistance) phenomena is a crucial aspect of cancer chemotherapy research. Artemisinin and its derivatives have been found to inhibit the proliferation of cancer cells in the microM range. They poorly inhibited the function of P-glycoprotein and did not inhibit the function of MRP1-protein. The concentrations required to inhibit by 50\% the function of P-glycoprotein are 110+/-5 microM. Artemisinin, artesunate and dihydroartemisinin efficiently decreased the mitochondrial membrane potential, leading to a decrease in intracellular ATP in all cell lines tested: by 30 to 50\% at 5 microM. Artemisinin, artesunate and dihydroartemisinin increased cytotoxicity of pirarubicin and doxorubicin in P-glycoprotein-overexpressing K562/adr, and in MRP1-overexpressing GLC4/adr, with the delta(0.5) ranging from 200 to 860 nM, but not in their corresponding drug-sensitive cell lines. In this range of concentrations these compounds did not decrease the function of P-glycoprotein, suggesting a mechanism by which the drugs did not reverse MDR phenomenon at the P-glycoprotein level but at the mitochondrial level.
This article was published in Biol Pharm Bull and referenced in International Journal of Inflammation, Cancer and Integrative Therapy

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