[Synergistic killing effect of arsenic trioxide combined with curcumin on KG1a cells].

作者：Jiaxin Fan, Yingjian Zeng, Jian-Wei Wu, Zhang-Qiu Li, Yuanming Li, Rong Zheng, Guangyang Weng, Kunyuan Guo · 发表于：PubMed · 年份：2014 · DOI：10.7534/j.issn.1009-2137.2014.05.015 · 被引用次数：4 · 研究领域：Retinoids in leukemia and cellular processes、Synthesis and Characterization of Heterocyclic Compounds、Synthesis and biological activity

This study was aimed to explore the effect of arsenic trioxide combined with curcumin on proliferation and apoptosis of KG1a cells and its potential mechanism. The cell survival rate was mesured by MTT; colony formation capacity was examined by methylcellulose colony formation test; flow cytometry was used to analyse the cell surface molecules, cell apoptosis rate and cell cycle; the cell morphology was observed with Wright-Giemsa staining and the protein expression of BCL-2, BAX, PARP was detected by Western blot. The results showed that the phenotype of KG1a cells was CD34(+)CD38(-), while the phenotype of HL-60 cell was CD34(+)CD38(+). The former possessed a stronger colony ability than the latter. Effect of curcumin and arsenic trioxide alone on cell proliferation and inhibition was in dose-dependent manner. Compared with single drug-treatment group, the cell survival rate and colony number were lower, and the apoptosis rate was higher in combined drug-treatment group. Protein expression of BCL-2 and PARP was upregulated, while the protein expression of PARP was downregulated in the combined treatment group. It is concluded that compared with HL-60 cells, KG1a cells are the earlier leukemia stem/progenitor cells. Arsenic trioxide combined with curcumin can effectively inhibit the KG1a cell proliferation and induce apoptosis, which may be associated with the downregulation of BCL-2 and PARP protein expression and the upregulation of BAX protein expression.