Costunolide enhances sensitivity of K562/ADR chronic myeloid leukemia cells to doxorubicin through PI3K/Akt pathway
Costunolide enhances sensitivity of K562/ADR chronic myeloid leukemia cells to doxorubicin through PI3K/Akt pathway
复制标题
DOI：
10.1002/ptr.6355
复制
发表时间：
2019-06-01
影响因子：
7.2
通讯作者：
Yang, Chunhui
中科院分区：
文献类型：
--
作者：
Cai, Hong;Li, Liangjun;Yang, Chunhui
木香烃内酯是一种萜烯内酯，是从旋覆花中提取的一种小分子单体，据报道对多种癌细胞系具有抗增殖作用。本研究旨在观察复方甘草酸苷对K562/ADR慢性粒细胞白血病细胞对阿霉素敏感性的影响。CCK-8法检测复方甘草酸苷的抗增殖作用。采用流式细胞术和Western blot方法研究其抗白血病作用机制。Costuntandine通过抑制PI 3 K/Akt通路、激活Caspases 3、切割聚ADP核糖聚合酶和下调P-糖蛋白表达，显著增强阿霉素诱导的K562/ADR细胞抗增殖活性。这些结果表明，costunetamine可能是一个有效的治疗药物对慢性粒细胞白血病。
Costunolide, a sesquiterpene lactone, a small molecular monomer extracted from Inula helenium, has been reported to possess antiproliferative effects on several cancer cell lines. The current study was designed to evaluate the effect of costunolide on sensitivity of K562/ADR chronic myeloid leukemia cells to doxorubicin. The antiproliferative effect of costunolide was assessed by CCK-8 assay. Flow cytometry and Western blot were used to examine the mechanisms of antileukemia action. Costunolide dramatically enhanced doxorubicin-induced antiproliferative activity against K562/ADR cells through inhibition of PI3K/Akt pathway, activation of caspases 3, cleavage of poly (ADP-ribose) polymerase, and downregulation of p-glycoprotein expression. These results demonstrate that costunolide may be a potent therapeutic agent against CML.