Department of Bioengineering, Stanford University, Stanford, CA, 94305, USA.
Department of Orthopaedic Surgery, Stanford University School of Medicine, Stanford, CA, 94305, USA.
Adv Healthc Mater. 2023 Jan;12(1):e2202147. doi: 10.1002/adhm.202202147. Epub 2022 Nov 16.
Glioblastoma multiforme (GBM) is the most prevalent and aggressive brain tumor in adults. Hydrogels have been employed as 3D in vitro culture models to elucidate how matrix cues such as stiffness and degradation drive GBM progression and drug responses. Recently, viscoelasticity has been identified as an important niche cue in regulating stem cell differentiation and morphogenesis in 3D. Brain is a viscoelastic tissue, yet how viscoelasticity modulates GBM fate and drug response remains largely unknown. Using dynamic hydrazone crosslinking chemistry, a poly(ethylene-glycol)-based hydrogel system with brain-mimicking stiffness and tunable stress relaxation is reported to interrogate the role of viscoelasticity on GBM fates in 3D. The hydrogel design allows tuning stress relaxation without changing stiffness, biochemical ligand density, or diffusion. The results reveal that increasing stress relaxation promotes invasive GBM behavior, such as cell spreading, migration, and GBM stem-like cell marker expression. Furthermore, increasing stress relaxation enhances GBM proliferation and drug sensitivity. Stress-relaxation induced changes on GBM fates and drug response are found to be mediated through the cytoskeleton and transient receptor potential vanilloid-type 4. These results highlight the importance of incorporating viscoelasticity into 3D in vitro GBM models and provide novel insights into how viscoelasticity modulates GBM cell fates.
多形性胶质母细胞瘤(GBM)是成人中最常见和侵袭性最强的脑肿瘤。水凝胶已被用作 3D 体外培养模型,以阐明基质线索(如刚度和降解)如何驱动 GBM 的进展和药物反应。最近,粘弹性已被确定为调节 3D 中干细胞分化和形态发生的重要生态位线索。大脑是一种粘弹性组织,但粘弹性如何调节 GBM 的命运和药物反应在很大程度上尚不清楚。本研究使用动态腙交联化学,报道了一种具有脑模拟刚度和可调应力松弛的聚(乙二醇)基水凝胶系统,用于研究粘弹性对 3D 中 GBM 命运的作用。水凝胶设计允许在不改变刚度、生化配体密度或扩散的情况下调整应力松弛。结果表明,增加应力松弛会促进侵袭性 GBM 行为,如细胞扩散、迁移和 GBM 干细胞样细胞标志物的表达。此外,增加应力松弛会增强 GBM 的增殖和药物敏感性。研究发现,应力松弛诱导的 GBM 命运和药物反应的变化是通过细胞骨架和瞬时受体电位香草素 4 介导的。这些结果强调了将粘弹性纳入 3D 体外 GBM 模型的重要性,并为粘弹性如何调节 GBM 细胞命运提供了新的见解。