Role of angiopoietins in mesothelioma progression.


Journal

Cytokine
ISSN: 1096-0023
Titre abrégé: Cytokine
Pays: England
ID NLM: 9005353

Informations de publication

Date de publication:
06 2019
Historique:
received: 22 06 2018
revised: 03 08 2018
accepted: 08 08 2018
pubmed: 12 9 2018
medline: 9 7 2020
entrez: 12 9 2018
Statut: ppublish

Résumé

Anti-angiogenic treatment has been recently shown to be clinically beneficial for mesothelioma patients. Angiopoietins-1 and -2 are key regulators of tumor angiogenesis. Ang-1 is mainly known to promote angiogenesis and vessel stability, while Ang-2 could serve as an antagonist of Ang-1 causing vessel regression and destabilization or enhance angiogenesis in a context-dependent manner. We hypothesized that Ang-1 would promote and Ang2 would halt experimental mesothelioma by affecting tumor angiogenesis. To examine the effects of angiopoietins in mesothelioma angiogenesis and in vivo growth we constructed Ang-1 or Ang-2 overexpressing AE17 and AB1 mesothelioma cells and implanted them in the respective syngeneic animals. We also explored the clinical relevance of our observations using the human tumoral mRNAseq data available in the TCGA database. Ang-1 promotes mesothelioma angiogenesis and growth while the effect of Ang-2 is context-dependent. Low Ang-1 levels in human mesotheliomas are associated with the epitheloid subtype. Tumors of high Ang-1, or concurrent high Ang-2 and VEGF expression present high PECAM-1 and CDH5 expression, markers of vascularity and vascular stability, respectively. Our results highlight the importance of angiopoietins in mesothelioma pathophysiology and pave the way for the clinical development of novel anti-angiogenic strategies.

Sections du résumé

BACKGROUND AND OBJECTIVE
Anti-angiogenic treatment has been recently shown to be clinically beneficial for mesothelioma patients. Angiopoietins-1 and -2 are key regulators of tumor angiogenesis. Ang-1 is mainly known to promote angiogenesis and vessel stability, while Ang-2 could serve as an antagonist of Ang-1 causing vessel regression and destabilization or enhance angiogenesis in a context-dependent manner. We hypothesized that Ang-1 would promote and Ang2 would halt experimental mesothelioma by affecting tumor angiogenesis.
METHODS
To examine the effects of angiopoietins in mesothelioma angiogenesis and in vivo growth we constructed Ang-1 or Ang-2 overexpressing AE17 and AB1 mesothelioma cells and implanted them in the respective syngeneic animals. We also explored the clinical relevance of our observations using the human tumoral mRNAseq data available in the TCGA database.
RESULTS AND CONCLUSIONS
Ang-1 promotes mesothelioma angiogenesis and growth while the effect of Ang-2 is context-dependent. Low Ang-1 levels in human mesotheliomas are associated with the epitheloid subtype. Tumors of high Ang-1, or concurrent high Ang-2 and VEGF expression present high PECAM-1 and CDH5 expression, markers of vascularity and vascular stability, respectively. Our results highlight the importance of angiopoietins in mesothelioma pathophysiology and pave the way for the clinical development of novel anti-angiogenic strategies.

Identifiants

pubmed: 30201261
pii: S1043-4666(18)30341-7
doi: 10.1016/j.cyto.2018.08.006
pii:
doi:

Substances chimiques

Angiopoietin-1 0
Angiopoietin-2 0
Platelet Endothelial Cell Adhesion Molecule-1 0
RNA, Messenger 0
Vascular Endothelial Growth Factor A 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

99-106

Informations de copyright

Copyright © 2018 Elsevier Ltd. All rights reserved.

Auteurs

Sophia Magkouta (S)

"Marianthi Simou Laboratory", 1st Department of Critical Care and Pulmonary Medicine, National and Kapodistrian University of Athens, School of Medicine, Evangelismos Hospital, 10675 Athens, Greece. Electronic address: smagkouta@med.uoa.gr.

Androniki Kollintza (A)

"Marianthi Simou Laboratory", 1st Department of Critical Care and Pulmonary Medicine, National and Kapodistrian University of Athens, School of Medicine, Evangelismos Hospital, 10675 Athens, Greece.

Charalampos Moschos (C)

"Marianthi Simou Laboratory", 1st Department of Critical Care and Pulmonary Medicine, National and Kapodistrian University of Athens, School of Medicine, Evangelismos Hospital, 10675 Athens, Greece.

Magdalini Spella (M)

Laboratory for Molecular Respiratory Carcinogenesis, Department of Physiology, Faculty of Medicine, University of Patras, 26504 Rio, Greece.

Ioannis Skianis (I)

Applied Econometrics & Data Analysis, Department of Statistics, Athens University of Economic & Business, Athens, Greece.

Apostolos Pappas (A)

"Marianthi Simou Laboratory", 1st Department of Critical Care and Pulmonary Medicine, National and Kapodistrian University of Athens, School of Medicine, Evangelismos Hospital, 10675 Athens, Greece.

Maria-Eleni Vazakidou (ME)

"Marianthi Simou Laboratory", 1st Department of Critical Care and Pulmonary Medicine, National and Kapodistrian University of Athens, School of Medicine, Evangelismos Hospital, 10675 Athens, Greece.

Georgios Stathopoulos (G)

Laboratory for Molecular Respiratory Carcinogenesis, Department of Physiology, Faculty of Medicine, University of Patras, 26504 Rio, Greece; Comprehensive Pneumology Center (CPC) and Institute for Lung Biology and Disease (iLBD), University Hospital, Ludwig-Maximilians University and Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), 81377 Munich, Germany.

Ioannis Kalomenidis (I)

"Marianthi Simou Laboratory", 1st Department of Critical Care and Pulmonary Medicine, National and Kapodistrian University of Athens, School of Medicine, Evangelismos Hospital, 10675 Athens, Greece.

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Classifications MeSH