Genistein modulates the decreased drug accumulation in non-P-glycoprotein mediated multidrug resistant tumour cells | Zendy

C. H. M. Versantvoort | Zendy; GJ Schuurhuis | Zendy; H. M. Pinedo | Zendy; CA Eekman | Zendy; C.M. Kuiper | Zendy; J. Lankelma | Zendy; H J Broxterman | Zendy

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Genistein modulates the decreased drug accumulation in non-P-glycoprotein mediated multidrug resistant tumour cells

Author(s) -

C. H. M. Versantvoort,

GJ Schuurhuis,

H. M. Pinedo,

CA Eekman,

C.M. Kuiper,

J. Lankelma,

H J Broxterman

Publication year - 1993

Publication title -

british journal of cancer

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.833

H-Index - 236

eISSN - 1532-1827

pISSN - 0007-0920

DOI - 10.1038/bjc.1993.458

Subject(s) - genistein , efflux , p glycoprotein , multiple drug resistance , daunorubicin , pharmacology , cell culture , hl60 , biology , multidrug resistance associated protein 2 , abcg2 , atp binding cassette transporter , doxorubicin , chemistry , transporter , drug resistance , biochemistry , microbiology and biotechnology , leukemia , immunology , endocrinology , chemotherapy , genetics , gene

In tumour cells the pharmacological basis for multidrug resistance (MDR) often appears to be a reduced cellular cytostatic drug accumulation caused by the drug efflux protein, P-glycoprotein (Pgp MDR), or by other drug transporters (non-Pgp MDR). Here we report the reversal of the decreased daunorubicin (DNR) accumulation in five non-Pgp MDR cell lines (GLC4/ADR, SW-1573/2R120, HT1080/DR4, MCF7/Mitox and HL60/ADR) by genistein. Genistein inhibited the enhanced DNR efflux in the GLC4/ADR cells. In these cells the decreased VP-16 accumulation was also reversed by genistein. Three other (iso)flavonoids biochanin A, apigenin and quercetin also increased the DNR accumulation in the GLC4/ADR cells. In contrast to the effects on non-Pgp MDR cells, 200 microM genistein did not increase the reduced DNR accumulation in three Pgp MDR cell lines (SW-1573/2R160, MCF7/DOX40 and KB8-5) or in the parental cell lines. In conclusion the use of genistein provides a means to probe non-Pgp related drug accumulation defects.

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