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Fu, L.W. et al.

Fu, Zhang, Liang, Yang, Pan,

The multidrug resistance of tumour cells was reversed by tetrandrine in vitro and in xenografts derived from human breast adenocarcinoma MCF-7/ adr cells.

Multidrug resistance (MDR) is one of the main obstacles limiting the efficacy of chemotherapy treatment of tumours. One of the main causes of MDR is linked to the overexpression of P-glycoprotein ( P-gp). This study aimed to characterise tetrandrine (Tet), a potent inhibitor of P-gp mediated MDR. Cytotoxicity was determined by the tetrazolium (MTT) assay. A MCF-7/ adr cell xenograft model was established to investigate the effect of Tet on reversing MDR in vivo. Mechanistic experiments were conducted to examine the uptake, efflux and accumulation of doxorubicin (Dox) and Fura-2, and to assess lipid membrane fluidity. Tet potentiated the cytotoxicity of Dox; a 20.4-fold reversal of resistance was achieved in the presence of 2.5 micromol/l of Tet. Accumulation and efflux studies with the P-gp substrates, Dox and Fura-2, demonstrated that Tet inhibited the P-gp-mediated drug efflux. In addition, Tet lowered cell membrane fluidity in a concentration-dependent manner. In mice bearing the MDR MCF-7/ adr cell xenografts, coadministration of Tet potentiated the antitumour activity of doxorubicin without a significant increase in toxicity. Tet was an extremely potent MDR modulator both in vitro and in vivo, without apparently enhancing the toxicity of the co-administered drugs. Hence, Tet holds great promise as a MDR modulator for the treatment of P-gp- mediated MDR cancers.[1]

References

The multidrug resistance of tumour cells was reversed by tetrandrine in vitro and in xenografts derived from human breast adenocarcinoma MCF-7/adr cells. Fu, L.W., Zhang, Y.M., Liang, Y.J., Yang, X.P., Pan, Q.C. Eur. J. Cancer (2002) [Pubmed]

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