2. Mechanisms of Action

migration

Definition

Cell migration is the directional movement of cells in response to external signals, crucial for embryonic development, wound healing, immune responses, and cancer metastasis. This complex process involves coordinated cytoskeletal reorganization, adhesion dynamics, and signal transduction cascades. Migration occurs through distinct phases: polarization, protrusion of leading edge structures (lamellipodia or filopodia), formation and maturation of focal adhesions, contractility of the cell body, and detachment of the trailing edge. Key molecular players include integrins, Rho GTPases (RhoA, Rac1, Cdc42), actin-binding proteins, and chemokine receptors. Understanding migration mechanisms is essential for developing therapies targeting cancer invasion, chronic inflammation, and impaired tissue repair.

Visualize migration in Nodes Bio

Researchers can map migration signaling networks by connecting chemokine receptors to downstream effectors like Rho GTPases, kinases, and cytoskeletal regulators. Network visualization reveals pathway crosstalk, identifies critical regulatory nodes, and highlights potential therapeutic targets. Users can overlay expression data to compare migratory versus stationary cell states, trace causal relationships from extracellular signals to phenotypic outcomes, and explore how genetic perturbations affect migration pathway integrity.

Visualization Ideas:

  • Chemokine receptor signaling cascades connecting to Rho GTPase regulatory networks
  • Integrin-focal adhesion complexes with mechanotransduction pathways
  • Comparative migration networks between normal and cancer cells showing pathway dysregulation
Request Beta Access →

Example Use Case

A cancer research team investigating melanoma metastasis uses network analysis to understand how CXCR4 chemokine receptor activation drives tumor cell migration. They construct a signaling network connecting CXCR4 to PI3K/AKT, MAPK pathways, and Rac1-mediated cytoskeletal remodeling. By integrating RNA-seq data from highly metastatic versus non-metastatic cell lines, they identify DOCK3 as an overexpressed guanine exchange factor promoting Rac1 activation. Network analysis reveals DOCK3's central position in the migration cascade, making it a promising therapeutic target for preventing metastasis.

Ready to visualize your research?

Join researchers using Nodes Bio for network analysis and visualization.

Request Beta Access