Division of Epigenetics, DKFZ-ZMBH Alliance, German Cancer Research Center, Heidelberg, Germany.
PLoS One. 2013;8(3):e59895. doi: 10.1371/journal.pone.0059895. Epub 2013 Mar 22.
Induction of differentiation in cancer stem cells by drug treatment represents an important approach for cancer therapy. The understanding of the mechanisms that regulate such a forced exit from malignant pluripotency is fundamental to enhance our knowledge of tumour stability. Certain nucleoside analogues, such as 2'-deoxy-5-azacytidine and 1β-arabinofuranosylcytosine, can induce the differentiation of the embryonic cancer stem cell line NTERA 2 D1 (NT2). Such induced differentiation is associated with drug-dependent DNA-damage, cellular stress and the proteolytic depletion of stem cell factors. In order to further elucidate the mode of action of these nucleoside drugs, we monitored differentiation-specific changes of the dielectric properties of growing NT2 cultures using electric cell-substrate impedance sensing (ECIS). We measured resistance values of untreated and retinoic acid treated NT2 cells in real-time and compared their impedance profiles to those of cell populations triggered to differentiate with several established substances, including nucleoside drugs. Here we show that treatment with retinoic acid and differentiation-inducing drugs can trigger specific, concentration-dependent changes in dielectric resistance of NT2 cultures, which can be observed as early as 24 hours after treatment. Further, low concentrations of nucleoside drugs induce differentiation-dependent impedance values comparable to those obtained after retinoic acid treatment, whereas higher concentrations induce proliferation defects. Finally, we show that impedance profiles of substance-induced NT2 cells and those triggered to differentiate by depletion of the stem cell factor OCT4 are very similar, suggesting that reduction of OCT4 levels has a dominant function for differentiation induced by nucleoside drugs and retinoic acid. The data presented show that NT2 cells have specific dielectric properties, which allow the early identification of differentiating cultures and real-time label-free monitoring of differentiation processes. This work might provide a basis for further analyses of drug candidates for differentiation therapy of cancers.
药物诱导癌症干细胞分化是癌症治疗的重要方法。了解调控这种恶性多能性强制退出的机制对于增强我们对肿瘤稳定性的认识至关重要。某些核苷类似物,如 2'-脱氧-5-氮杂胞苷和 1β-阿拉伯呋喃糖基胞嘧啶,可诱导胚胎癌细胞系 NTERA 2 D1(NT2)分化。这种诱导分化与药物依赖性 DNA 损伤、细胞应激和干细胞因子的蛋白水解耗竭有关。为了进一步阐明这些核苷药物的作用机制,我们使用细胞-基质阻抗传感(ECIS)监测生长中的 NT2 培养物分化特异性的介电特性变化。我们实时测量未处理和维甲酸处理的 NT2 细胞的电阻值,并将其阻抗谱与用几种已建立的物质(包括核苷药物)触发分化的细胞群体的阻抗谱进行比较。在这里,我们显示维甲酸和诱导分化药物的处理可以触发 NT2 培养物介电电阻的特异性、浓度依赖性变化,这些变化早在处理后 24 小时即可观察到。此外,低浓度的核苷药物诱导的分化依赖性阻抗值与维甲酸处理后获得的阻抗值相当,而较高浓度的药物则诱导增殖缺陷。最后,我们表明,诱导物质的 NT2 细胞的阻抗谱与通过耗尽干细胞因子 OCT4 触发分化的细胞的阻抗谱非常相似,这表明降低 OCT4 水平对核苷药物和维甲酸诱导的分化具有主导作用。所呈现的数据表明,NT2 细胞具有特定的介电特性,允许早期识别分化培养物并实时无标记监测分化过程。这项工作可能为进一步分析用于癌症分化治疗的药物候选物提供基础。