Ursolic acid induces HL60 monocytic differentiation and upregulates C/EBPβ expression by ERK pathway activation
Ursolic acid induces HL60 monocytic differentiation and upregulates C/EBPβ expression by ERK pathway activation
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DOI：
10.1097/cad.0b013e3283409673
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发表时间：
2011-02-01
影响因子：
2.3
通讯作者：
Xi, Tao
中科院分区：
文献类型：
--
作者：
Zhang, Ting;He, Yun-Mian;Xi, Tao
熊果酸（UA）是一种五环三萜类化合物，广泛分布于植物界，具有广泛的生物学作用。本研究通过形态学观察、硝基四氮唑蓝还原试验、CD 14和CD 11b表面抗原表达等方法，首次探讨了UA对人白血病HL 60细胞分化的作用及其机制。此外，尿酸激活细胞外信号调节激酶（ERK）途径，在剂量依赖性和时间依赖性的方式。用PD 98059抑制ERK通路的激活可显著阻断UA诱导的分化。与诱导分化一致，UA对CCAAT/增强子结合蛋白β的上调也被PD 98059消除。总之，本文报道的结果表明，UA可以促进HL 60细胞的单核细胞分化，并通过激活ERK通路增加CCAAT/增强子结合蛋白β的表达，这表明UA可能是一个潜在的候选人作为分化诱导剂用于白血病的治疗治疗。抗癌药物22：158-165（C）2011年威科健康垂直栏Lippincott威廉姆斯&威尔金斯。
Ursolic acid (UA), a pentacyclic triterpenoid compound, is widely distributed in the plant kingdom and has a broad range of biological effects. This study was carried out for the first time to investigate the potential role of UA in the differentiation of human leukemia HL60 cells and the underlying mechanisms in it. UA could induce differentiation of HL60 cells into the monocytic lineage, as assessed by the morphological change, nitroblue tetrazolium reduction assay, and expression of CD14 and CD11b surface antigens. Moreover, UA activated the extracellular signal-regulated kinase (ERK) pathway in both dose-dependent and time-dependent manners. Inhibiting ERK pathway activation with PD98059 could significantly block the differentiation induced by UA. Consistent with the induced differentiation, the upregulation of CCAAT/enhancer-binding protein beta by UA was also eliminated by PD98059. Taken together, the results reported here show that UA can promote the monocytic differentiation of HL60 cells and increase the expression of CCAAT/enhancer-binding protein beta by activating the ERK pathway, suggesting that UA could be a potential candidate as a differentiation-inducing agent for the therapeutic treatment of leukemia. Anti-Cancer Drugs 22:158-165 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.