CCL26 ‐Mediated Modulation of Endothelial Secretome by Hypoxia‐Induced Tumor‐Derived Exosomes Enhances Metastatic Progression in Head and Neck Cancer | Synapse
April 5, 2026Open Access
CCL26 ‐Mediated Modulation of Endothelial Secretome by Hypoxia‐Induced Tumor‐Derived Exosomes Enhances Metastatic Progression in Head and Neck Cancer
Key Points
The study aims to investigate how tumor-derived exosomes influence endothelial cell behavior through CCL26 under hypoxic conditions.
Analysis of endothelial secretome modifications
Exosome isolation from hypoxic tumor environments
CCL26 level measurement in endothelial cells
Elevated CCL26 levels in endothelial cells exposed to hypoxic tumor-derived exosomes
Enhanced tumor-supportive characteristics in endothelial cells
Increased metastatic progression observed in head and neck cancer models
Abstract
hiTDExs reprogram endothelial secretomes by elevating CCL26, promoting tumor-supportive phenotypes and driving metastatic progression in HNSCC.