Serveur d'exploration sur le lymphœdème

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Role of hypoxia and vascular endothelial growth factors in lymphangiogenesis

Identifieur interne : 000067 ( France/Analysis ); précédent : 000066; suivant : 000068

Role of hypoxia and vascular endothelial growth factors in lymphangiogenesis

Auteurs : Florent Morfoisse [France] ; Edith Renaud [France] ; Fransky Hantelys [France] ; Anne-Catherine Prats [France] ; Barbara Garmy-Susini [France]

Source :

RBID : PMC:4905355

Abstract

Hypoxia is a major condition for the induction of angiogenesis during tumor development but its role in lymphangiogenesis remains unclear. Blood and lymphatic vasculatures are stimulated by growth factors from the vascular endothelial family: the VEGFs. In this review, we investigate the role of hypoxia in the molecular regulation of synthesis of lymphangiogenic growth factors VEGF-A, VEGF-C, and VEGF-D. Gene expression can be regulated at transcriptional and translational levels by hypoxia. Despite strong regulation of DNA transcription induced by hypoxia-inducible factors (HIFs), the majority of cellular stresses such as hypoxia lead to inhibition of cap-dependent translation of the mRNA, resulting in downregulation of protein synthesis. Here, we describe how translation initiation of VEGF mRNAs is induced by hypoxia through an internal ribosome entry site (IRES)-dependent mechanism. Considering the implication of the lymphatic vasculature in metastatic dissemination, it seems crucial to understand the hypoxia-induced molecular regulation of lymphangiogenic growth factors to obtain new insights for cancer therapy.


Url:
DOI: 10.1080/23723556.2015.1024821
PubMed: 27308508
PubMed Central: 4905355


Affiliations:


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PMC:4905355

Le document en format XML

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<list>
<country>
<li>France</li>
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<name sortKey="Morfoisse, Florent" sort="Morfoisse, Florent" uniqKey="Morfoisse F" first="Florent" last="Morfoisse">Florent Morfoisse</name>
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<name sortKey="Renaud, Edith" sort="Renaud, Edith" uniqKey="Renaud E" first="Edith" last="Renaud">Edith Renaud</name>
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</tree>
</affiliations>
</record>

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