Tang-Schomer Min D, Bookland Markus J, Sargent Jack E, N Jackvony Taylor
UConn Health, Department of Pediatrics, 263 Farmington Avenue, Farmington, CT 06030, USA.
Connecticut Children's Medical Center, 282 Washington St., Hartford, CT 06106, USA.
Bioengineering (Basel). 2023 Jul 15;10(7):840. doi: 10.3390/bioengineering10070840.
Despite in vivo malignancy, ependymoma lacks cell culture models, thus limiting therapy development. Here, we used a tunable three-dimensional (3D) culture system to approximate the ependymoma microenvironment for recapitulating a patient's tumor in vitro. Our data showed that the inclusion of VEGF in serum-free, mixed neural and endothelial cell culture media supported the in vitro growth of all four ependymoma patient samples. The growth was driven by Nestin and Ki67 double-positive cells in a putative cancer stem cell niche, which was manifested as rosette-looking clusters in 2D and spheroids in 3D. The effects of extracellular matrix (ECM) such as collagen or Matrigel superseded that of the media conditions, with Matrigel resulting in the greater enrichment of Nestin-positive cells. When mixed with endothelial cells, the 3D co-culture models developed capillary networks resembling the in vivo ependymoma vasculature. The transcriptomic analysis of two patient cases demonstrated the separation of in vitro cultures by individual patients, with one patient's culture samples closely clustered with the primary tumor tissue. While VEGF was found to be necessary for preserving the transcriptomic features of in vitro cultures, the presence of endothelial cells shifted the gene's expression patterns, especially genes associated with ECM remodeling. The homeobox genes were mostly affected in the 3D in vitro models compared to the primary tumor tissue and between different 3D formats. These findings provide a basis for understanding the ependymoma microenvironment and enabling the further development of patient-derived in vitro ependymoma models for personalized medicine.
尽管室管膜瘤在体内具有恶性特征,但它缺乏细胞培养模型,这限制了治疗方法的开发。在此,我们使用了一种可调谐的三维(3D)培养系统来模拟室管膜瘤的微环境,以便在体外重现患者的肿瘤。我们的数据表明,在无血清、混合神经和内皮细胞的培养基中加入血管内皮生长因子(VEGF)可支持所有四个室管膜瘤患者样本的体外生长。这种生长由假定的癌症干细胞龛中的巢蛋白(Nestin)和Ki67双阳性细胞驱动,在二维中表现为玫瑰花结样簇,在三维中表现为球体。细胞外基质(ECM)如胶原蛋白或基质胶的作用超过了培养基条件的影响,基质胶导致巢蛋白阳性细胞的富集程度更高。当与内皮细胞混合时,3D共培养模型形成了类似于体内室管膜瘤脉管系统的毛细血管网络。对两个患者病例的转录组分析表明,体外培养物按个体患者分离,其中一名患者的培养样本与原发性肿瘤组织紧密聚集。虽然发现VEGF对于保留体外培养物的转录组特征是必要的,但内皮细胞的存在改变了该基因的表达模式,尤其是与ECM重塑相关的基因。与原发性肿瘤组织相比,以及在不同的3D形式之间,同源盒基因在3D体外模型中大多受到影响。这些发现为理解室管膜瘤微环境以及进一步开发用于个性化医疗的患者来源的体外室管膜瘤模型提供了基础。