Dihydroartemisinin-induced apoptosis in human acute monocytic leukemia cells

被引:14
|
作者
Cao, Jia-Tian [1 ]
Mo, Hui-Min [2 ,3 ]
Wang, Yue [1 ]
Zhao, Kai [2 ,3 ]
Zhang, Tian-Tian [1 ]
Wang, Chang-Qian [1 ]
Xu, Kai-Lin [2 ,3 ]
Han, Zhi-Hua [1 ]
机构
[1] Shanghai Jiao Tong Univ, Med Sch, Peoples Hosp 9, Dept Cardiol, 639 Zhizaoju Rd, Shanghai 200011, Peoples R China
[2] Xuzhou Med Univ, Inst Hematol, 99 West Huaihai Rd, Xuzhou 221002, Jiangsu, Peoples R China
[3] Xuzhou Med Univ, Affiliated Hosp, Dept Hematol, Xuzhou 221002, Jiangsu, Peoples R China
基金
中国国家自然科学基金;
关键词
dihydroartemisinin; acute monocytic leukemia; apoptosis; extracellular signal-regulated kinase; protein kinase B; caspase-3; ACUTE MYELOID-LEUKEMIA; THP-1; CELLS; PROLIFERATION; CYTOTOXICITY; PATHWAYS; PROMOTES; DIFFERENTIATION; DERIVATIVES; AUTOPHAGY; SURVIVAL;
D O I
10.3892/ol.2017.7644
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Dihydroartemisinin (DHA) is a derivative of artemisinin. The present study aimed to investigate whether DHA induces apoptosis in the THP-1 human acute monocytic leukemia cell line (AMoL), and to identify the relative molecular mechanisms. The results of the present study demonstrated that the viability of THP-1 cells were inhibited by DHA in a dose- and time-dependent manner, which was accompanied by morphological characteristics associated with apoptosis. After 24 h of 200 mu M DHA treatment, the proportion of apoptotic cells was significantly increased compared with the untreated controls (P<0.01). In addition, DHA downregulated the levels of B-cell lymphoma (Bcl)-2, protein kinase B (Akt) 1, Akt2 and Akt3 gene expression, and increased the expression of the Bcl-2-associated X protein apoptosis regulator. The protein expression of phospho-Akt and phospho-extracellular signal-regulated kinase (ERK) was also decreased, and the protein expression level of cleaved caspase-3 was increased following treatment with DHA. Therefore, DHA may induce apoptosis in the AMoL THP-1 cell line via currently unknown underlying molecular mechanisms, including the downregulation of ERK and Akt, and the activation of caspase-3.
引用
收藏
页码:3178 / 3184
页数:7
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