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Real-time Imaging of Endothelial Cell-cell Junctions During Neutrophil Transmigration Under Physiological Flow
Published on: August 14, 2014
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Localized translation regulates cell adhesion and transendothelial migration.
Jonathan Bergeman1, Alexia Caillier1, François Houle2
1Centre de Recherche sur le Cancer de l'Université Laval, Faculté de Médecine, Université Laval, Québec, Canada, G1V 0A6.
Journal of Cell Science
|September 18, 2016
Summary
Cancer cells undergoing epithelial-to-mesenchymal transition (EMT) can alter their adhesion. Spreading initiation centers (SICs) regulate cell adhesion strength, acting as a checkpoint for metastatic dissemination.
Area of Science:
- Cell biology
- Cancer research
- Molecular biology
Background:
- Epithelial-to-mesenchymal transition (EMT) enables cancer cells to invade tissues.
- Metastatic cells gain plasticity through mesenchymal-to-amoeboid transition (MAT).
- Cell adhesion is critical for cancer cell dissemination.
Purpose of the Study:
- To investigate the role of spreading initiation centers (SICs) in cell adhesion.
- To understand the regulation of metastatic cell plasticity and dissemination.
- To identify novel checkpoints in cancer cell adhesion.
Main Methods:
- Observation of cell morphology and adhesion dynamics.
- Characterization of spreading initiation centers (SICs).
- Analysis of polyadenylated RNA localization and translation within SICs.
Main Results:
- Adhering cells form SICs with amoeboid cell characteristics.
- SIC-induced adhesion recapitulates amoeboid-to-mesenchymal transition (AMT) events.
- Polyadenylated RNAs in SICs regulate metastatic cell adhesion potential.
Conclusions:
- SICs represent a novel regulatory mechanism for cell adhesion.
- Blocking RNA translation in SICs impairs metastatic cell adhesion.
- This identifies a new checkpoint controlling cell adhesion strength and cancer cell dissemination.
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