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Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
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Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However,...
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In animal cells, the extracellular matrix allows cells within tissues to withstand external stresses and transmits signals from the outside of the cell to the inside. The extracellular matrix is extensive, and its composition varies between different types of tissues. For example, the reticular fibers and ground substance make up the ECM in loose connective tissue, while collagen and bone minerals make up the ECM of bone tissue. 
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The extracellular matrix or ECM holds cells together to form a tissue and allows the cells within the tissue to communicate. ECM comprises proteins such as fibronectin, collagen, laminin, etc. The most abundant protein in this space is collagen. Collagen fibers are interwoven with carbohydrate-containing protein molecules called proteoglycans. ECM allows cell migration and provides a structural scaffold at cell adhesion that anchors the cell when the extracellular matrix proteins interact with...
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Related Experiment Video

Updated: Mar 15, 2026

Quantitative Measurement of Invadopodia-mediated Extracellular Matrix Proteolysis in Single and Multicellular Contexts
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The Extracellular Matrix Regulates Invasion in Fusion-Negative Rhabdomyosarcoma via YAP-PIEZO1 Signaling Axis.

Yuanzhong Pan1, Juha Kim1, Brian M Wong1

  • 1Cancer and Blood Disease Institute, Children's Hospital Los Angeles, Los Angeles, CA 90027, USA.

Cancers
|March 14, 2026
PubMed
Summary

Extracellular matrix density drives fusion-negative rhabdomyosarcoma (FNRMS) invasion via the YAP-PIEZO1 pathway. Targeting this mechanosensitive axis offers a potential therapeutic strategy for aggressive FNRMS.

Keywords:
PIEZO1YAPcalcium signalingextracellular matrixfusion-negative rhabdomyosarcomainvasionspheroid

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A Cancer Cell Spheroid Assay to Assess Invasion in a 3D Setting
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Area of Science:

  • Oncology
  • Cell Biology
  • Biophysics

Background:

  • Fusion-negative rhabdomyosarcoma (FNRMS) is the most common pediatric soft-tissue sarcoma.
  • Tumor invasion in FNRMS correlates with poor prognosis and recurrence, but mechanisms are poorly understood.
  • Investigating the role of extracellular matrix density in FNRMS progression via mechano-transduction.

Purpose of the Study:

  • To elucidate the mechanism by which extracellular matrix density influences FNRMS cell invasion.
  • To identify key molecular players in the mechano-transduction pathway regulating FNRMS progression.
  • To explore the therapeutic potential of targeting identified pathways in FNRMS.

Main Methods:

  • Utilized three-dimensional spheroid invasion assays with FNRMS cells in varying collagen densities.
  • Employed immunofluorescence, gene sequencing, live-cell calcium imaging, and pharmacological inhibition.
  • Focused on the YAP-PIEZO1 signaling axis.

Main Results:

  • High extracellular matrix density significantly increased FNRMS invasive spreading and YAP nuclear localization.
  • YAP activation promoted invasion, while inhibition attenuated matrix-enhanced invasion.
  • Identified PIEZO1 as a direct YAP target; PIEZO1-dependent calcium influx was crucial for invasion.
  • Elevated PIEZO1 expression correlated with poorer patient survival.
  • Targeting YAP inhibited calcium flux and FNRMS invasion.

Conclusions:

  • Established a YAP-PIEZO1 signaling axis linking extracellular matrix density to FNRMS invasion.
  • This mechanosensitive pathway represents a potential therapeutic vulnerability in aggressive FNRMS.
  • Findings suggest novel therapeutic strategies targeting mechano-transduction in FNRMS.