Exosomes from EGFR-Mutated Adenocarcinoma Induce a Hybrid EMT and MMP9-Dependant Tumor Invasion

Exosomes, a class of extra cellular nano-sized vesicles (EVs), and their contents have gained attention as potential sources of information on tumor detection and regulatory drivers of tumor progression and metastasis. The effect of exosomes isolated from patients with an Epidermal Growth Factor Rec...

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Bibliographic Details
Published in:Cancers 2022-08, Vol.14 (15), p.3776
Main Authors: Jouida, Amina, O’Callaghan, Marissa, Mc Carthy, Cormac, Fabre, Aurelie, Nadarajan, Parthiban, Keane, Michael P.
Format: Article
Language:English
Subjects:
1-Phosphatidylinositol 3-kinase
Adenocarcinoma
AKT protein
Antibodies
Biopsy
Biotechnology
Cell adhesion molecules
Cellulose
E-cadherin
Epidermal growth factor
Epidermal growth factor receptors
Epithelial cells
Exosomes
Gelatinase B
Gene expression
Kinases
Lung cancer
Matrix metalloproteinase
Medical prognosis
Mesenchyme
Metalloproteinase
Metastases
Metastasis
Morphology
Mutation
Non-small cell lung carcinoma
Proteins
Rapamycin
Small cell lung carcinoma
TOR protein
Transmission electron microscopy
Tumors
Vesicles
Vimentin
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Summary:Exosomes, a class of extra cellular nano-sized vesicles (EVs), and their contents have gained attention as potential sources of information on tumor detection and regulatory drivers of tumor progression and metastasis. The effect of exosomes isolated from patients with an Epidermal Growth Factor Receptor (EGFR)-mutated adenocarcinoma on the promotion of epithelial–mesenchymal transition (EMT) and invasion were examined. Exosomes derived from serum of patients with EGFR-mutated non-small cell lung cancer (NSCLC) mediate the activation of the Phosphoinositide 3-kinase (PI3K)/AKT/ mammalian target of rapamycin (mTOR) pathway and induce an invasion through the up-regulation of matrix metalloproteinase-9 (MMP-9) in A549 cells. We observed a significant increase in the expression of vimentin, a mesenchymal marker, while retaining the epithelial characteristics, as evidenced by the unaltered levels of E-cadherin and Epithelial cell adhesion molecule (EPCAM). We also observed an increase of nuclear factor erythroid 2-related factor 2 (NFR2) and P-cadherin expression, markers of hybrid EMT. Exosomes derived from EGFR-mutated adenocarcinoma serum could be a potential mediator of hybrid EMT and tumor invasion. Understanding how cancerous cells communicate and interact with their environment via exosomes will improve our understanding of lung cancer progression and metastasis formation.
ISSN:2072-6694
2072-6694
DOI:10.3390/cancers14153776