Vascular permeability changes involved in tumor metastasis.
Jonathan García-Román1, Alejandro Zentella-Dehesa
1Unidad de Bioquímica, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubiran, Vasco de Quiroga No. 15, Colonia Sección XVI, Delegación Tlalpan, CP 04510 México City, Mexico.
Cancer Letters
|March 19, 2013
Summary
Cancer cells metastasize by increasing vascular permeability, similar to inflammatory responses. Tumor cells release factors that weaken endothelial junctions, facilitating their spread to new tissues.
Area of Science:
- Oncology
- Cell Biology
- Physiology
Background:
- Cancer cell extravasation mirrors leukocyte recruitment during inflammation.
- Cancer cells must disrupt interendothelial junctions to breach the endothelial barrier.
- Tumor cells utilize soluble factors to enhance vascular permeability for metastasis.
Purpose of the Study:
- To summarize current knowledge on vascular permeability changes in tumor metastasis.
- To highlight the role of tumor-derived soluble factors in metastasis.
- To discuss the signaling pathways involved in interendothelial junction disassembly.
Main Methods:
- Literature review of current research on cancer cell extravasation.
- Analysis of tumor-derived factors affecting vascular permeability.
- Summary of signaling pathways, including Src kinase, in junction disassembly.
Main Results:
- Cancer cells employ mechanisms similar to inflammatory cells for extravasation.
- Vasoactive compounds like VEGF, Angptl4, CCL2, and SDF-1 are implicated.
- Src kinase is a common signaling element in interendothelial junction disassembly.
Conclusions:
- Tumor cells possess a diverse array of soluble factors to increase vascular permeability.
- Disruption of interendothelial junctions is crucial for tumor cell colonization.
- Understanding these mechanisms is key to developing anti-metastatic therapies.
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