Dissecting TGF-β-induced glioblastoma invasion with engineered hyaluronic acid hydrogels

IF 6.6 3区 医学 Q1 ENGINEERING, BIOMEDICAL
K. Y. Amofa, Katherine Michelle Patterson, Jessica Ortiz, Sanjay Kumar
{"title":"Dissecting TGF-β-induced glioblastoma invasion with engineered hyaluronic acid hydrogels","authors":"K. Y. Amofa, Katherine Michelle Patterson, Jessica Ortiz, Sanjay Kumar","doi":"10.1063/5.0203213","DOIUrl":null,"url":null,"abstract":"Glioma stem cells (GSCs) contribute to rapid cellular invasion in glioblastoma (GBM). Transforming growth factor-β (TGF-β) has been strongly implicated in supporting key GSC functions, including stemness, immunosuppression, and resistance. Although TGF-β is well-known as a driver of cancer invasion, how TGF-β supports the invasion of GSCs is not well understood. Progress in understanding mechanisms of TGF-β-driven invasion in GSC-derived tumors has been limited by an absence of three-dimensional (3D) culture systems that support TGF-β-stimulated invasion. Here, we show that 3D hyaluronic acid (HA) matrices can address this need. We perform bioinformatic analysis of human glioma datasets, which reveals progressive enrichment of TGF-β-related gene expression with increasingly aggressive glioma grade and GBM subtype. We then experimentally screen the invasion of a panel of human GSC spheroids through a set of 3D matrix systems, including collagen I, Matrigel, and HA, and find that only HA recapitulates TGF-β-induced invasion. We then show that GSCs differ in their ability to invade HA in a way that can be predicted from TGF-β receptor 2 expression and SMAD2 phosphorylation. GSC spheroid invasion depends strongly on the presence of RGD peptides on the HA backbone but is surprisingly independent of matrix metalloprotease degradability. Finally, we demonstrate that TGF-β stimulates invasion through SMAD-dependent signaling, consistent with recent observations that TGF-β/SMAD signals drive tumor microtube formation and invasion. Our work supports further development of HA as a matrix platform for dissecting contributions of TGF-β and other cytokines to GBM invasion and screening of cytokine-dependent invasion in human tumors.","PeriodicalId":46288,"journal":{"name":"APL Bioengineering","volume":null,"pages":null},"PeriodicalIF":6.6000,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"APL Bioengineering","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1063/5.0203213","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"ENGINEERING, BIOMEDICAL","Score":null,"Total":0}
引用次数: 0

Abstract

Glioma stem cells (GSCs) contribute to rapid cellular invasion in glioblastoma (GBM). Transforming growth factor-β (TGF-β) has been strongly implicated in supporting key GSC functions, including stemness, immunosuppression, and resistance. Although TGF-β is well-known as a driver of cancer invasion, how TGF-β supports the invasion of GSCs is not well understood. Progress in understanding mechanisms of TGF-β-driven invasion in GSC-derived tumors has been limited by an absence of three-dimensional (3D) culture systems that support TGF-β-stimulated invasion. Here, we show that 3D hyaluronic acid (HA) matrices can address this need. We perform bioinformatic analysis of human glioma datasets, which reveals progressive enrichment of TGF-β-related gene expression with increasingly aggressive glioma grade and GBM subtype. We then experimentally screen the invasion of a panel of human GSC spheroids through a set of 3D matrix systems, including collagen I, Matrigel, and HA, and find that only HA recapitulates TGF-β-induced invasion. We then show that GSCs differ in their ability to invade HA in a way that can be predicted from TGF-β receptor 2 expression and SMAD2 phosphorylation. GSC spheroid invasion depends strongly on the presence of RGD peptides on the HA backbone but is surprisingly independent of matrix metalloprotease degradability. Finally, we demonstrate that TGF-β stimulates invasion through SMAD-dependent signaling, consistent with recent observations that TGF-β/SMAD signals drive tumor microtube formation and invasion. Our work supports further development of HA as a matrix platform for dissecting contributions of TGF-β and other cytokines to GBM invasion and screening of cytokine-dependent invasion in human tumors.
用工程透明质酸水凝胶剖析TGF-β诱导的胶质母细胞瘤侵袭
胶质瘤干细胞(GSCs)有助于胶质母细胞瘤(GBM)的快速细胞侵袭。转化生长因子-β(TGF-β)与支持胶质瘤干细胞的主要功能密切相关,包括干性、免疫抑制和抵抗力。尽管众所周知 TGF-β 是癌症侵袭的驱动因素,但人们对 TGF-β 如何支持 GSCs 的侵袭还不甚了解。由于缺乏支持TGF-β刺激侵袭的三维(3D)培养系统,人们对TGF-β驱动的GSC衍生肿瘤侵袭机制的了解一直受到限制。在这里,我们展示了三维透明质酸(HA)基质可以满足这一需求。我们对人类胶质瘤数据集进行了生物信息学分析,结果表明,随着胶质瘤侵袭性等级和 GBM 亚型的增加,TGF-β 相关基因表达逐渐丰富。然后,我们通过实验筛选了一组人类 GSC 球体在一系列三维基质系统(包括胶原 I、Matrigel 和 HA)中的侵袭情况,发现只有 HA 能再现 TGF-β 诱导的侵袭。然后,我们发现 GSC 侵袭 HA 的能力与 TGF-β 受体 2 表达和 SMAD2 磷酸化预测的方式不同。GSC球体的侵袭在很大程度上取决于HA骨架上RGD肽的存在,但令人惊讶的是,它与基质金属蛋白酶的降解性无关。最后,我们证明了 TGF-β 通过 SMAD 依赖性信号刺激侵袭,这与最近观察到的 TGF-β/SMAD 信号驱动肿瘤微管形成和侵袭是一致的。我们的工作支持进一步开发 HA 作为基质平台,用于分析 TGF-β 和其他细胞因子对 GBM 侵袭的贡献,以及筛选人类肿瘤中依赖细胞因子的侵袭。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
APL Bioengineering
APL Bioengineering ENGINEERING, BIOMEDICAL-
CiteScore
9.30
自引率
6.70%
发文量
39
审稿时长
19 weeks
期刊介绍: APL Bioengineering is devoted to research at the intersection of biology, physics, and engineering. The journal publishes high-impact manuscripts specific to the understanding and advancement of physics and engineering of biological systems. APL Bioengineering is the new home for the bioengineering and biomedical research communities. APL Bioengineering publishes original research articles, reviews, and perspectives. Topical coverage includes: -Biofabrication and Bioprinting -Biomedical Materials, Sensors, and Imaging -Engineered Living Systems -Cell and Tissue Engineering -Regenerative Medicine -Molecular, Cell, and Tissue Biomechanics -Systems Biology and Computational Biology
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信