Göttlich Claudia, Müller Lena C, Kunz Meik, Schmitt Franziska, Walles Heike, Walles Thorsten, Dandekar Thomas, Dandekar Gudrun, Nietzer Sarah L
Department of Tissue Engineering and Regenerative Medicine (TERM), University Hospital Wuerzburg.
Department of Bioinformatics, University Wuerzburg.
J Vis Exp. 2016 Apr 6(110):e53885. doi: 10.3791/53885.
In the present study, we combined an in vitro 3D lung tumor model with an in silico model to optimize predictions of drug response based on a specific mutational background. The model is generated on a decellularized porcine scaffold that reproduces tissue-specific characteristics regarding extracellular matrix composition and architecture including the basement membrane. We standardized a protocol that allows artificial tumor tissue generation within 14 days including three days of drug treatment. Our article provides several detailed descriptions of 3D read-out screening techniques like the determination of the proliferation index Ki67 staining's, apoptosis from supernatants by M30-ELISA and assessment of epithelial to mesenchymal transition (EMT), which are helpful tools for evaluating the effectiveness of therapeutic compounds. We could show compared to 2D culture a reduction of proliferation in our 3D tumor model that is related to the clinical situation. Despite of this lower proliferation, the model predicted EGFR-targeted drug responses correctly according to the biomarker status as shown by comparison of the lung carcinoma cell lines HCC827 (EGFR -mutated, KRAS wild-type) and A549 (EGFR wild-type, KRAS-mutated) treated with the tyrosine-kinase inhibitor (TKI) gefitinib. To investigate drug responses of more advanced tumor cells, we induced EMT by long-term treatment with TGF-beta-1 as assessed by vimentin/pan-cytokeratin immunofluorescence staining. A flow-bioreactor was employed to adjust culture to physiological conditions, which improved tissue generation. Furthermore, we show the integration of drug responses upon gefitinib treatment or TGF-beta-1 stimulation - apoptosis, proliferation index and EMT - into a Boolean in silico model. Additionally, we explain how drug responses of tumor cells with a specific mutational background and counterstrategies against resistance can be predicted. We are confident that our 3D in vitro approach especially with its in silico expansion provides an additional value for preclinical drug testing in more realistic conditions than in 2D cell culture.
在本研究中,我们将体外3D肺肿瘤模型与计算机模型相结合,以基于特定的突变背景优化药物反应预测。该模型是在脱细胞猪支架上构建的,该支架再现了包括基底膜在内的细胞外基质组成和结构的组织特异性特征。我们标准化了一种方案,该方案允许在14天内生成人工肿瘤组织,包括三天的药物治疗。我们的文章提供了几种3D读出筛选技术的详细描述,如增殖指数Ki67染色的测定、通过M30-ELISA从培养上清液中检测凋亡以及上皮-间质转化(EMT)的评估,这些都是评估治疗化合物有效性的有用工具。与二维培养相比,我们可以证明我们的3D肿瘤模型中的增殖减少,这与临床情况相关。尽管增殖较低,但该模型根据生物标志物状态正确预测了表皮生长因子受体(EGFR)靶向药物反应,如用酪氨酸激酶抑制剂(TKI)吉非替尼处理的肺癌细胞系HCC827(EGFR突变,KRAS野生型)和A549(EGFR野生型,KRAS突变)的比较所示。为了研究更晚期肿瘤细胞的药物反应,我们通过波形蛋白/全细胞角蛋白免疫荧光染色评估,用转化生长因子-β-1长期处理诱导EMT。采用流动生物反应器将培养条件调整到生理条件,这改善了组织生成。此外,我们展示了吉非替尼治疗或转化生长因子-β-1刺激后的药物反应——凋亡、增殖指数和EMT——整合到一个布尔计算机模型中。此外,我们解释了如何预测具有特定突变背景的肿瘤细胞的药物反应以及针对耐药性的应对策略。我们相信,我们的3D体外方法,尤其是其计算机扩展,在比二维细胞培养更现实的条件下为临床前药物测试提供了额外价值。