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Interplay between Matrix Viscoelasticity and Integrin Engagement Modulates Cancer-Associated Fibroblast States.

Yunyun Wang1, Zixuan Zhao2, Nicholas Ching Wei Ho1

  • 1Department of Biomedical Engineering, National University of Singapore, Kent Ridge, 119276, Singapore.

Advanced Healthcare Materials
|July 29, 2025
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Summary
This summary is machine-generated.

Researchers found that matrix properties like hydrogel viscoelasticity and cell adhesion influence cancer-associated fibroblast (CAF) states, specifically myofibroblastic CAFs (myCAFs) and inflammatory CAFs (iCAFs). This discovery aids in developing better preclinical models for cancer research.

Keywords:
JAK/STAT signaling pathwaycancer‐associated fibroblastviscoelasticity

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Area of Science:

  • Cancer Biology
  • Biomaterials Science
  • Cellular Plasticity

Background:

  • Single-cell transcriptomics reveals cancer-associated fibroblasts (CAFs) are heterogeneous, with distinct subsets exhibiting unique functions.
  • Understanding CAF subset function and developing targeted therapies are hindered by the lack of preclinical models that control CAF heterogeneity in vitro.
  • Previous research suggests CAF plasticity is influenced by culture matrix parameters.

Purpose of the Study:

  • To investigate how hydrogel viscoelasticity and integrin engagement modulate the plasticity of encapsulated CAFs.
  • To determine if these matrix parameters can specifically skew CAFs towards myofibroblastic CAF (myCAF) or inflammatory CAF (iCAF) states.
  • To establish novel in vitro models for studying CAF heterogeneity and function.

Main Methods:

  • Utilized alginate hydrogels to encapsulate patient-derived CAFs.
  • Varied hydrogel viscoelasticity and controlled cell adhesion (integrin engagement).
  • Analyzed CAF morphology and transcriptomic profiles using single-cell transcriptomics.
  • Investigated the role of the JAK/STAT signaling pathway in CAF state modulation.

Main Results:

  • Patient-derived CAFs adopted distinct morphologies and transcriptomic profiles resembling myCAF or iCAF states based on hydrogel viscoelasticity and cell adhesion.
  • Demonstrated that matrix properties significantly influence CAF plasticity in vitro.
  • Identified the JAK/STAT signaling pathway as crucial for iCAF maintenance and a potential target for altering CAF states.

Conclusions:

  • Matrix viscoelasticity and integrin engagement are key regulators of CAF states in vitro.
  • Developed novel in vitro models that controllably recapitulate CAF heterogeneity.
  • These models offer a valuable tool for understanding CAF functions and advancing the development of CAF-targeted cancer therapies.