دورية أكاديمية
أعرض في EDS

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

التفاصيل البيبلوغرافية
العنوان: Dissecting TGF-β-induced glioblastoma invasion with engineered hyaluronic acid hydrogels.
المؤلفون: Amofa KY, Patterson KM; Department of Bioengineering, University of California, Berkeley, California 94720, USA., Ortiz J, Kumar S
المصدر: APL bioengineering [APL Bioeng] 2024 Jun 13; Vol. 8 (2), pp. 026125. Date of Electronic Publication: 2024 Jun 13 (Print Publication: 2024).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: AIP Publishing Country of Publication: United States NLM ID: 101726398 Publication Model: eCollection Cited Medium: Internet ISSN: 2473-2877 (Electronic) Linking ISSN: 24732877 NLM ISO Abbreviation: APL Bioeng Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: Melville, NY : AIP Publishing, [2017]-
مستخلص: 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.
Competing Interests: The authors have no conflicts to disclose.
(© 2024 Author(s).)
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معلومات مُعتمدة: P30 CA016672 United States CA NCI NIH HHS; R01 CA247970 United States CA NCI NIH HHS; R01 GM122375 United States GM NIGMS NIH HHS; R01 CA214749 United States CA NCI NIH HHS; R01 CA260443 United States CA NCI NIH HHS; P50 CA127001 United States CA NCI NIH HHS
تواريخ الأحداث: Date Created: 20240619 Latest Revision: 20240621
رمز التحديث: 20240621
مُعرف محوري في PubMed: PMC11184968
DOI: 10.1063/5.0203213
PMID: 38894960
قاعدة البيانات: MEDLINE
الوصف
تدمد:2473-2877
DOI:10.1063/5.0203213