Apoptosis Sensitization by Euphorbia Factor L1 in ABCB1-Mediated Multidrug Resistant K562/ADR Cells

Molecules

Jian-Ye Zhang¹  Min-Ting Lin²  Tao Yi¹  Yi-Na Tang¹  Lan-Lan Fan¹  Xi-Cheng He¹  Zhong-Zhen Zhao¹ 

[1] School of Chinese Medicine, Hong Kong Baptist University, 7 Baptist University Road, Kowloon Tong, Kowloon, Hong Kong; E-Mails:;School of Pharmaceutical Sciences, Guangzhou Medical University, 195 Dongfeng Road West, Guangzhou 510000, China; E-Mail:

关键词: ABCB1;    multidrug resistance;    apoptosis;    Euphorbia factor L1;   

DOI  :  10.3390/molecules181012793

来源: mdpi

【 摘 要 】

In this article, reversal activities of Euphorbia factor L1 (EFL1) against ABCB1-mediated multidrug resistance (MDR) and apoptosis sensitization in K562/ADR cells are reported. EFL1 decreased the IC₅₀ values of anticancer agents in K562/ADR cells over-expressing ABCB1. However, EFL1 did not affect the IC₅₀ values of anticancer agents in sensitive K562 cells. Additionally, EFL1 increased the intracellular accumulation of rhodamine 123 and doxorubicin in K562/ADR cells without affecting their accumulation in K562 cells. Furthermore, EFL1 sensitized the apoptosis triggered by vincristine in K562/ADR cells via mitochondrial pathway, as confirmed by Annexin V-FITC/PI detection and western blot. At the same time, EFL1 did not influence the apoptosis induced by vincristine in K562 cells. Western blot results showed that EFL1 did not affect the phosphorylation level of AKT and ERK in K562 and K562/ADR cells. Finally, EFL1 did not down-regulate protein expression of ABCB1.

【 授权许可】

CC BY   
© 2013 by the authors; licensee MDPI, Basel, Switzerland.