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Molecules 2016, 21(2), 183; doi:10.3390/molecules21020183

Alisol F 24 Acetate Enhances Chemosensitivity and Apoptosis of MCF-7/DOX Cells by Inhibiting P-Glycoprotein-Mediated Drug Efflux

1
Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China
2
Tianjin International Joint Academy of Biomedicine, Tianjin 300457, China
*
Author to whom correspondence should be addressed.
Academic Editor: Helena Vasconcelos
Received: 30 November 2015 / Revised: 26 January 2016 / Accepted: 28 January 2016 / Published: 4 February 2016
(This article belongs to the Special Issue New Approaches to Counteract Drug Resistance in Cancer)
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Abstract

Multidrug resistance (MDR) is a prime reason for numerous failed oncotherapy approaches. In the present study, we investigated whether Alisol F 24 acetate (ALI) could reverse the MDR of MCF-7/DOX cells, a multidrug-resistant human breast cancer cell line. We found that ALI was a potent P-glycoprotein (P-gp) inhibitor, in the Caco-2-monolayer cell model. ALI showed a significant and concentration-dependent cytotoxic effect on MCF-7/DOX cells in combination with doxorubicin by increasing intracellular accumulation and inducing nuclear migration of doxorubicin. However, ALI had no such effect on MCF-7 cells. In addition, ALI also promoted doxorubicin-induced early apoptosis of MCF-7/DOX cells in a time-dependent manner. These results suggest that ALI can enhance chemosensitivity of doxorubicin and reinforce its anti-cancer effect by increasing its uptake, especially inducing its nuclear accumulation in MCF-7/DOX cells. Therefore, ALI could be developed as a potential MDR-reversing agent in cancer chemotherapy in further study. View Full-Text
Keywords: alisol F 24-acetate (ALI); multidrug resistance (MDR); doxorubicin; P-glycoprotein (P-gp) alisol F 24-acetate (ALI); multidrug resistance (MDR); doxorubicin; P-glycoprotein (P-gp)
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Pan, G.; Li, T.; Zeng, Q.; Wang, X.; Zhu, Y. Alisol F 24 Acetate Enhances Chemosensitivity and Apoptosis of MCF-7/DOX Cells by Inhibiting P-Glycoprotein-Mediated Drug Efflux. Molecules 2016, 21, 183.

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