Jung Sang Yoon, Kim Chulwon, Kim Wan-Seok, Lee Seok-Geun, Lee Jun-Hee, Shim Bum Sang, Kim Sung-Hoon, Ahn Kyoo Seok, Ahn Kwang Seok
College of Korean Medicine, Kyung Hee University, 1 Hoegidong, Dongdaemun-gu, Seoul, 130-701, Korea.
Botanical Drug Laboratory, R&D Headquarter, Korea Ginseng Corporation, Daejeon, 305-805, Korea.
Phytother Res. 2015 Jul;29(7):1062-72. doi: 10.1002/ptr.5347. Epub 2015 Apr 8.
Although imatinib mesylate (IM) in the treatment of chronic myelogenous leukemia (CML) remains the best example of successful targeted therapy, majority of patients with CML suffer its toxicity profile and develop chemoresistance to existing therapeutic agents. Thus, there is a need to develop novel alternative therapies for the treatment of CML. Here, we investigated whether Korean red ginseng extract (KRGE) could suppress the proliferation and induce chemosensitization in human CML cells. Also, we used a human phospho-antibody array containing 46 antibodies against signaling molecules to examine a subset of phosphorylation events after treatment. Korean red ginseng extract broadly suppressed the proliferation of five different cell lines, but KRGE was found to be the most potent inducer of apoptosis against KBM-5 cells. It also abrogated the expression of Bcl-2 (B-cell lymphoma 2), Bcl-xL (B-cell lymphoma-extra large), survivin, inhibitors of apoptosis protein 1/2, COX-2 (Cyclooxygenase-2), cyclin D1, matrix metalloproteinase-9, and VEGF (Vascular endothelial growth factor), as well as upregulated the expression of pro-apoptotic gene products. Interestingly, KRGE also enhanced the cytotoxic and apoptotic effect of IM in KBM-5 cells. The combination treatment of KRGE and IM caused pronounced suppression of p38 and signal transducer and activator of transcription 5 phosphorylation and induced phosphorylation of p53 compared with the individual treatment. Our results demonstrate that KRGE can enhance the anticancer activity of IM and may have a substantial potential in the treatment of CML.
虽然甲磺酸伊马替尼(IM)治疗慢性粒细胞白血病(CML)仍是成功靶向治疗的最佳范例,但大多数CML患者会遭受其毒性反应,并对现有治疗药物产生化疗耐药性。因此,需要开发新的替代疗法来治疗CML。在此,我们研究了韩国红参提取物(KRGE)是否能抑制人CML细胞的增殖并诱导化疗增敏作用。此外,我们使用了一种包含46种针对信号分子的抗体的人磷酸化抗体芯片,以检测治疗后磷酸化事件的一个子集。韩国红参提取物广泛抑制了五种不同细胞系的增殖,但发现KRGE是对KBM-5细胞最有效的凋亡诱导剂。它还消除了Bcl-2(B细胞淋巴瘤2)、Bcl-xL(B细胞淋巴瘤-超大)、生存素、凋亡抑制蛋白1/2、COX-2(环氧化酶-2)、细胞周期蛋白D1、基质金属蛋白酶-9和VEGF(血管内皮生长因子)的表达,并上调了促凋亡基因产物的表达。有趣的是,KRGE还增强了IM对KBM-5细胞的细胞毒性和凋亡作用。与单独治疗相比,KRGE和IM联合治疗显著抑制了p38以及信号转导和转录激活因子5的磷酸化,并诱导了p53的磷酸化。我们的结果表明,KRGE可以增强IM的抗癌活性,在CML治疗中可能具有巨大潜力。