LymphedemaV1, PubMed, Curation, bibRecord, 001493

Novel action and mechanism of auranofin in inhibition of vascular endothelial growth factor receptor-3-dependent lymphangiogenesis.

Identifieur interne : 001493 ( PubMed/Curation ); précédent : 001492; suivant : 001494

Novel action and mechanism of auranofin in inhibition of vascular endothelial growth factor receptor-3-dependent lymphangiogenesis.

Auteurs : Xiaodong Chen ; Huanjiao Jenny Zhou ; Qunhua Huang ; Lin Lu ; Wang Min [États-Unis]

Source :

Anti-cancer agents in medicinal chemistry [ 1875-5992 ] ; 2014.

RBID : pubmed:24913775

Descripteurs français

English descriptors

KwdEn :
- Apoptosis (drug effects), Auranofin (pharmacology), Cell Line, Cell Movement (drug effects), Cell Proliferation (drug effects), Cell Survival (drug effects), Endothelial Cells (cytology), Endothelial Cells (drug effects), Humans, Lymphangiogenesis (drug effects), Lysosomes (metabolism), Mitogen-Activated Protein Kinase 14 (metabolism), NF-kappa B (metabolism), Signal Transduction (drug effects), Thioredoxin-Disulfide Reductase (metabolism), Vascular Endothelial Growth Factor Receptor-3 (metabolism).
MESH :
- chemical , metabolism : Mitogen-Activated Protein Kinase 14, NF-kappa B, Thioredoxin-Disulfide Reductase, Vascular Endothelial Growth Factor Receptor-3.
- chemical , pharmacology : Auranofin.
- cytology : Endothelial Cells.
- drug effects : Apoptosis, Cell Movement, Cell Proliferation, Cell Survival, Endothelial Cells, Lymphangiogenesis, Signal Transduction.
- metabolism : Lysosomes.
- Cell Line, Humans.

Abstract

Auranofin is a gold compound initially developed for the treatment of rheumatoid arthritis. Recent data suggest that auranofin has promise in the treatment of other inflammatory and proliferative diseases. However, the mechanisms of action of auranofin have not been well defined. In the present study, we identify vascular endothelial growth factor receptor-3 (VEGFR3), an endothelial cell (EC) surface receptor essential for angiogiogenesis and lymphangiogenesis, as a novel target of auranofin. In both primary EC and EC cell lines, auranofin induces downregulation of VEGFR3 in a dose-dependent manner. Auranofin at high doses (≥1 µM) decreases cellular survival protein thioredoxin reductase (TrxR2), TrxR2-dependent Trx2 and transcription factor NF-κB whereas increases stress signaling p38MAPK, leading to EC apoptosis. However, auranofin at low doses (≤0.5 µM) specifically induces downregulation of VEGFR3 and VEGFR3-mediated EC proliferation and migration, two critical steps required for in vivo lymphangiogenesis. Mechanistically, we show that auranofin-induced VEGFR3 downregulation is blocked by antioxidant N-acetyl-L-cysteine (NAC) and lysosome inhibitor chloroquine, but is promoted by proteasomal inhibitor MG132. These results suggest that auranofin induces VEGFR3 degradation through a lysosome-dependent pathway. Auranofin may be a potent therapeutic agent for the treatment of lymphangiogenesis-dependent diseases such as lymphedema and cancer metastasis.

PubMed: 24913775

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<term>Auranofin (pharmacology)</term>
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<term>Cell Proliferation (drug effects)</term>
<term>Cell Survival (drug effects)</term>
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<term>Endothelial Cells (drug effects)</term>
<term>Humans</term>
<term>Lymphangiogenesis (drug effects)</term>
<term>Lysosomes (metabolism)</term>
<term>Mitogen-Activated Protein Kinase 14 (metabolism)</term>
<term>NF-kappa B (metabolism)</term>
<term>Signal Transduction (drug effects)</term>
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<term>Auranofine (pharmacologie)</term>
<term>Cellules endothéliales ()</term>
<term>Cellules endothéliales (cytologie)</term>
<term>Facteur de transcription NF-kappa B (métabolisme)</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Lymphangiogenèse ()</term>
<term>Lysosomes (métabolisme)</term>
<term>Mitogen-Activated Protein Kinase 14 (métabolisme)</term>
<term>Mouvement cellulaire ()</term>
<term>Prolifération cellulaire ()</term>
<term>Récepteur-3 au facteur croissance endothéliale vasculaire (métabolisme)</term>
<term>Survie cellulaire ()</term>
<term>Thioredoxin-disulfide reductase (métabolisme)</term>
<term>Transduction du signal ()</term>
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<term>Cell Movement</term>
<term>Cell Proliferation</term>
<term>Cell Survival</term>
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<term>Cellules endothéliales</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Lymphangiogenèse</term>
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<front><div type="abstract" xml:lang="en">Auranofin is a gold compound initially developed for the treatment of rheumatoid arthritis. Recent data suggest that auranofin has promise in the treatment of other inflammatory and proliferative diseases. However, the mechanisms of action of auranofin have not been well defined. In the present study, we identify vascular endothelial growth factor receptor-3 (VEGFR3), an endothelial cell (EC) surface receptor essential for angiogiogenesis and lymphangiogenesis, as a novel target of auranofin. In both primary EC and EC cell lines, auranofin induces downregulation of VEGFR3 in a dose-dependent manner. Auranofin at high doses (≥1 µM) decreases cellular survival protein thioredoxin reductase (TrxR2), TrxR2-dependent Trx2 and transcription factor NF-κB whereas increases stress signaling p38MAPK, leading to EC apoptosis. However, auranofin at low doses (≤0.5 µM) specifically induces downregulation of VEGFR3 and VEGFR3-mediated EC proliferation and migration, two critical steps required for in vivo lymphangiogenesis. Mechanistically, we show that auranofin-induced VEGFR3 downregulation is blocked by antioxidant N-acetyl-L-cysteine (NAC) and lysosome inhibitor chloroquine, but is promoted by proteasomal inhibitor MG132. These results suggest that auranofin induces VEGFR3 degradation through a lysosome-dependent pathway. Auranofin may be a potent therapeutic agent for the treatment of lymphangiogenesis-dependent diseases such as lymphedema and cancer metastasis.</div>
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<Abstract><AbstractText>Auranofin is a gold compound initially developed for the treatment of rheumatoid arthritis. Recent data suggest that auranofin has promise in the treatment of other inflammatory and proliferative diseases. However, the mechanisms of action of auranofin have not been well defined. In the present study, we identify vascular endothelial growth factor receptor-3 (VEGFR3), an endothelial cell (EC) surface receptor essential for angiogiogenesis and lymphangiogenesis, as a novel target of auranofin. In both primary EC and EC cell lines, auranofin induces downregulation of VEGFR3 in a dose-dependent manner. Auranofin at high doses (≥1 µM) decreases cellular survival protein thioredoxin reductase (TrxR2), TrxR2-dependent Trx2 and transcription factor NF-κB whereas increases stress signaling p38MAPK, leading to EC apoptosis. However, auranofin at low doses (≤0.5 µM) specifically induces downregulation of VEGFR3 and VEGFR3-mediated EC proliferation and migration, two critical steps required for in vivo lymphangiogenesis. Mechanistically, we show that auranofin-induced VEGFR3 downregulation is blocked by antioxidant N-acetyl-L-cysteine (NAC) and lysosome inhibitor chloroquine, but is promoted by proteasomal inhibitor MG132. These results suggest that auranofin induces VEGFR3 degradation through a lysosome-dependent pathway. Auranofin may be a potent therapeutic agent for the treatment of lymphangiogenesis-dependent diseases such as lymphedema and cancer metastasis.</AbstractText>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName>
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   |texte=   Novel action and mechanism of auranofin in inhibition of vascular endothelial growth factor receptor-3-dependent lymphangiogenesis.
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Novel action and mechanism of auranofin in inhibition of vascular endothelial growth factor receptor-3-dependent lymphangiogenesis.

Novel action and mechanism of auranofin in inhibition of vascular endothelial growth factor receptor-3-dependent lymphangiogenesis.

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