Illuminating breast cancer invasion: diverse roles for cell–cell interactions

KJ Cheung, AJ Ewald - Current opinion in cell biology, 2014 - Elsevier
KJ Cheung, AJ Ewald
Current opinion in cell biology, 2014Elsevier
Highlights•Cancer invasion is accomplished through interactions among distinct cell
types.•Both epithelial–epithelial and epithelial–stromal interactions regulate
invasion.•Metastasis can occur without a molecular epithelial to mesenchymal
transition.•Multiple different mechanisms have been identified to promote
invasion.Metastasis begins when tumors invade into surrounding tissues. In breast cancer,
the study of cell interactions has provided fundamental insights into this complex process …
Highlights
  • Cancer invasion is accomplished through interactions among distinct cell types.
  • Both epithelial–epithelial and epithelial–stromal interactions regulate invasion.
  • Metastasis can occur without a molecular epithelial to mesenchymal transition.
  • Multiple different mechanisms have been identified to promote invasion.
Metastasis begins when tumors invade into surrounding tissues. In breast cancer, the study of cell interactions has provided fundamental insights into this complex process. Powerful intravital and 3D organoid culture systems have emerged that enable biologists to model the complexity of cell interactions during cancer invasion in real-time. Recent studies utilizing these techniques reveal distinct mechanisms through which multiple cancer cell and stromal cell subpopulations interact, including paracrine signaling, direct cell–cell adhesion, and remodeling of the extracellular matrix. Three cell interaction mechanisms have emerged to explain how breast tumors become invasive: epithelial–mesenchymal transition, collective invasion, and the macrophage–tumor cell feedback loop. Future work is needed to distinguish whether these mechanisms are mutually exclusive or whether they cooperate to drive metastasis.
Elsevier