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ECM Cross-Linking Regulates Invadopodia Dynamics.

Kamyar Esmaeili Pourfarhangi1, Aviv Bergman2, Bojana Gligorijevic3

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|March 29, 2018
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Summary
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Cancer cells dynamically switch between invadopodia states for invasion. ECM cross-linking and β1-integrin binding control these dynamics, impacting cancer cell metastasis.

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Area of Science:

  • Cell Biology
  • Cancer Research
  • Biophysics

Background:

  • Invadopodia are crucial for cancer cell invasion and metastasis.
  • While invadopodia assembly is studied, their dynamics and interaction with the extracellular matrix (ECM) are less understood.
  • Cancer cell invasion involves complex interactions between cellular machinery and the physical properties of the ECM.

Purpose of the Study:

  • To investigate the dynamics of invadopodia in invasive cancer cells.
  • To explore how extracellular matrix (ECM) cross-linking and β1-integrin binding influence invadopodia dynamics and cancer cell invasion.
  • To understand the relationship between physical ECM properties and cancer cell behavior.

Main Methods:

  • Time-lapse microscopy and mathematical modeling of invasive cancer cells.
  • Manipulation of ECM cross-linking density in 2D and 3D cultures.
  • Inhibition of β1-integrin signaling.

Main Results:

  • Cancer cells exhibit an "invadopodia state" (stasis) and a "migration state" (translocation).
  • ECM cross-linking and β1-integrin binding modulate the duration of these states.
  • Intermediate ECM cross-linking (0.39) maximizes invadopodia dynamics and ECM degradation via MT1-MMP.
  • Both very high and very low ECM cross-linking reduce invadopodia dynamics and degradation.

Conclusions:

  • β1-integrin-ECM binding nonlinearly translates ECM physical properties into cancer cell behavior dynamics.
  • ECM cross-linking influences invadopodia protrusion-retraction cycles and MT1-MMP delivery.
  • Targeting environmental factors like ECM cross-linking may offer novel therapeutic strategies to inhibit cancer metastasis.