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Mechanism of Tetrandrine in Combination with Droloxifen To Reverse Multidrug Resistance in Leukemia.

Baoan Chen, Ailing Su, Feng Gao, Jian Cheng, Jia-Hua Ding, Chong Gao, Yun-Yu Sun, Jun Wang, Gang Zhao, Ning-Na Chen, Huihui Zhao, Xiao-Ping Pei

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Abstract

Objective: The study aims to investigate the effect of Tetrandrine (Tetrandrine, Tet) in combination with Droloxifen (Droloxifen, DRL) on the expression of NF-κB(nuclear factor kappaB) of K562 and K562/A02 cell lines and the reversal mechanism of this combination. Method: The activation of NF-κB in K562 and K562/A02 cell lines and the effect of Tet,DRL alone or in combination on NF-κB were determined with Immunocytochemistry and Western blotting respectively. Results: K562/A02 cells displayed higher level of NF-κB protein expression than their parental K562 cells; The application of Tet or DRL alone or in combination had no effect on NF-κB expression in K562 cells at 6h and 12h; Tet and DRL used alone or in combination could significantly down-regulate NF-κB protein expression in nucleaus of K562/A02 cells. The effect was more significant in combination of Tet and DRL than the application of single drug. This decrease became more significant at 12h than at 6h. Conclusions: Activation of NF-κB may be involved in the mechanism of MDR of K562/A02 cell line; Inhibition of NF-κB activation may be involved in the mechanism of multidrug resistance reversal to K562/A02 line of Tet and DRL.

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What this paper is about

Objective: The study aims to investigate the effect of Tetrandrine (Tetrandrine, Tet) in combination with Droloxifen (Droloxifen, DRL) on the expression of NF-κB(nuclear factor kappaB) of K562 and K562/A02 cell lines and the reversal mechanism of this combination. Method: The activation of NF-κB in K562 and K562/A02 cell lines and the effect of Tet,DRL alone or in combination on NF-κB were determined with Immunocytochemistry and Western blotting respectively. Results: K562/A02 cells displayed higher level of NF-κB protein expression than their parental K562 cells; The application of Tet or DRL alone or in combination had no effect on NF-κB expression in K562 cells at 6h and 12h; Tet and DRL used alone or in combination could significantly down-regulate NF-κB protein expression in nucleaus of K562/A02 cells. The effect was more significant in combination of Tet and DRL than the application of single drug. This decrease became more significant at 12h than at 6h. Conclusions: Activation of NF-κB may be involved in the mechanism of MDR of K562/A02 cell line; Inhibition of NF-κB activation may be involved in the mechanism of multidrug resistance reversal to K562/A02 line of Tet and DRL.

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Available abstract

Objective: The study aims to investigate the effect of Tetrandrine (Tetrandrine, Tet) in combination with Droloxifen (Droloxifen, DRL) on the expression of NF-κB(nuclear factor kappaB) of K562 and K562/A02 cell lines and the reversal mechanism of this combination. Method: The activation of NF-κB in K562 and K562/A02 cell lines and the effect of Tet,DRL alone or in combination on NF-κB were determined with Immunocytochemistry and Western blotting respectively. Results: K562/A02 cells displayed higher level of NF-κB protein expression than their parental K562 cells; The application of Tet or DRL alone or in combination had no effect on NF-κB expression in K562 cells at 6h and 12h; Tet and DRL used alone or in combination could significantly down-regulate NF-κB protein expression in nucleaus of K562/A02 cells. The effect was more significant in combination of Tet and DRL than the application of single drug. This decrease became more significant at 12h than at 6h. Conclusions: Activation of NF-κB may be involved in the mechanism of MDR of K562/A02 cell line; Inhibition of NF-κB activation may be involved in the mechanism of multidrug resistance reversal to K562/A02 line of Tet and DRL.

Key concepts: Tetrandrine, K562 cells, Multiple drug resistance, Cell culture, Molecular biology, Biology, Blot, Pharmacology

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Mechanism of Tetrandrine in Combination with Droloxifen To Reverse Multidrug Resistance in Leukemia. — Research Paper | ScholarLens