Intravasation-On-µDevice (INVADE): Engineering Dynamic Vascular Interfaces to Study Cancer Cell Intravasation.

Jiang, F; Zhang, Y; Fang, G; Wang, Y; Dupuy, A; Jin, J; Shen, Y; Lim, KS; Wang, Y; Zhang, YS; Cho, A-N; Lu, H; Ju, LA

Intravasation-On-µDevice (INVADE): Engineering Dynamic Vascular Interfaces to Study Cancer Cell Intravasation.

Jiang, F Zhang, Y Fang, G

Wang, Y Dupuy, A Jin, J Shen, Y Lim, KS Wang, Y Zhang, YS Cho, A-N Lu, H Ju, LA

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Publisher:: Wiley
Publication Type:: Journal Article
Citation:: Adv Mater, 2025, 37, (26), pp. e2501466
Issue Date:: 2025-07

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Field	Value	Language
dc.contributor.author	Jiang, F
dc.contributor.author	Zhang, Y
dc.contributor.author	Fang, G https://orcid.org/0000-0001-5457-7030
dc.contributor.author	Wang, Y
dc.contributor.author	Dupuy, A
dc.contributor.author	Jin, J
dc.contributor.author	Shen, Y
dc.contributor.author	Lim, KS
dc.contributor.author	Wang, Y
dc.contributor.author	Zhang, YS
dc.contributor.author	Cho, A-N
dc.contributor.author	Lu, H
dc.contributor.author	Ju, LA
dc.date.accessioned	2025-08-11T03:52:40Z
dc.date.available	2025-08-11T03:52:40Z
dc.date.issued	2025-07
dc.identifier.citation	Adv Mater, 2025, 37, (26), pp. e2501466
dc.identifier.issn	0935-9648
dc.identifier.issn	1521-4095
dc.identifier.uri	http://hdl.handle.net/10453/189339
dc.description.abstract	Cancer metastasis begins with intravasation, where cancer cells enter blood vessels through complex interactions with the endothelial barrier. Understanding this process remains challenging due to the lack of physiologically relevant models. Here, INVADE (Intravasation-on-µDevice), a biomimetic microfluidic platform, is presented, enabling high-throughput analysis of cancer cell intravasation under controlled conditions. This engineered platform integrates 23 parallel niche chambers with an endothelialized channel, providing both precise microenvironmental control and optical accessibility for real-time visualization. Using this platform, distinct intravasation mechanisms are uncovered: MCF-7 cells exhibit collective invasion, while MDA-MB-231 cells demonstrate an interactive mode with three functionally distinct subpopulations. A previously unknown epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) switch is We discovered during intravasation, where MDA-MB-231 cells initially increase Vimentin expression before undergoing a 2.3 fold decrease over 96 h alongside a 1.5 fold increase in epithelial cell adhesion molecule (EpCAM). Remarkably, endothelial cells directly suppress cancer cell mesenchymal properties, as evidenced by a 4.6 fold reduction in Vimentin expression compared to mono-cultures. Additionally, bilateral cancer-endothelial interactions are revealed, aggressive cancer cells induce significant intercellular adhesion molecule-1 (ICAM-1) upregulation in endothelium. The INVADE platform represents an engineering advancement for studying complex cell-cell interactions with implications for understanding metastatic mechanisms.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	Wiley
dc.relation.ispartof	Adv Mater
dc.relation.isbasedon	10.1002/adma.202501466
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	02 Physical Sciences, 03 Chemical Sciences, 09 Engineering
dc.subject.classification	Nanoscience & Nanotechnology
dc.subject.classification	34 Chemical sciences
dc.subject.classification	40 Engineering
dc.subject.classification	51 Physical sciences
dc.subject.mesh	Humans
dc.subject.mesh	Cell Line, Tumor
dc.subject.mesh	Epithelial Cell Adhesion Molecule
dc.subject.mesh	Epithelial-Mesenchymal Transition
dc.subject.mesh	MCF-7 Cells
dc.subject.mesh	Neoplasm Invasiveness
dc.subject.mesh	Vimentin
dc.subject.mesh	MDA-MB-231 Cells
dc.subject.mesh	Cell Line, Tumor
dc.subject.mesh	Humans
dc.subject.mesh	Neoplasm Invasiveness
dc.subject.mesh	Vimentin
dc.subject.mesh	Epithelial-Mesenchymal Transition
dc.subject.mesh	MCF-7 Cells
dc.subject.mesh	Epithelial Cell Adhesion Molecule
dc.subject.mesh	MDA-MB-231 Cells
dc.title	Intravasation-On-µDevice (INVADE): Engineering Dynamic Vascular Interfaces to Study Cancer Cell Intravasation.
dc.type	Journal Article
utslib.citation.volume	37
utslib.location.activity	Germany
utslib.for	02 Physical Sciences
utslib.for	03 Chemical Sciences
utslib.for	09 Engineering
pubs.organisational-group	University of Technology Sydney
pubs.organisational-group	University of Technology Sydney/Faculty of Engineering and Information Technology
pubs.organisational-group	University of Technology Sydney/Faculty of Engineering and Information Technology/School of Biomedical Engineering
utslib.copyright.status	open_access	*
dc.rights.license	This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/
dc.date.updated	2025-08-11T03:52:36Z
pubs.issue	26
pubs.publication-status	Published
pubs.volume	37
utslib.citation.issue	26

Abstract:

Cancer metastasis begins with intravasation, where cancer cells enter blood vessels through complex interactions with the endothelial barrier. Understanding this process remains challenging due to the lack of physiologically relevant models. Here, INVADE (Intravasation-on-µDevice), a biomimetic microfluidic platform, is presented, enabling high-throughput analysis of cancer cell intravasation under controlled conditions. This engineered platform integrates 23 parallel niche chambers with an endothelialized channel, providing both precise microenvironmental control and optical accessibility for real-time visualization. Using this platform, distinct intravasation mechanisms are uncovered: MCF-7 cells exhibit collective invasion, while MDA-MB-231 cells demonstrate an interactive mode with three functionally distinct subpopulations. A previously unknown epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) switch is We discovered during intravasation, where MDA-MB-231 cells initially increase Vimentin expression before undergoing a 2.3 fold decrease over 96 h alongside a 1.5 fold increase in epithelial cell adhesion molecule (EpCAM). Remarkably, endothelial cells directly suppress cancer cell mesenchymal properties, as evidenced by a 4.6 fold reduction in Vimentin expression compared to mono-cultures. Additionally, bilateral cancer-endothelial interactions are revealed, aggressive cancer cells induce significant intercellular adhesion molecule-1 (ICAM-1) upregulation in endothelium. The INVADE platform represents an engineering advancement for studying complex cell-cell interactions with implications for understanding metastatic mechanisms.

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http://hdl.handle.net/10453/189339