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The long noncoding RNA MALAT1 promotes tumor-driven angiogenesis by up-regulating pro-angiogenic gene expression.

Identifieur interne : 002212 ( PubMed/Curation ); précédent : 002211; suivant : 002213

The long noncoding RNA MALAT1 promotes tumor-driven angiogenesis by up-regulating pro-angiogenic gene expression.

Auteurs : Andrew E. Tee [Australie] ; Bing Liu [Australie] ; Renhua Song [Australie] ; Jinyan Li [Australie] ; Eddy Pasquier [France] ; Belamy B. Cheung [Australie] ; Cizhong Jiang [République populaire de Chine] ; Glenn M. Marshall [Australie] ; Michelle Haber [Australie] ; Murray D. Norris [Australie] ; Jamie I. Fletcher [Australie] ; Marcel E. Dinger [Australie] ; Tao Liu [Australie]

Source :

Oncotarget [ 1949-2553 ] ; 2016.

RBID : pubmed:26848616

Descripteurs français

English descriptors

KwdEn :
- Apoptosis, Blotting, Western, Cell Movement, Cell Proliferation, Cells, Cultured, Enzyme-Linked Immunosorbent Assay, Fibroblast Growth Factor 2 (genetics), Fibroblast Growth Factor 2 (metabolism), Gene Expression Regulation, Neoplastic, Human Umbilical Vein Endothelial Cells (cytology), Human Umbilical Vein Endothelial Cells (metabolism), Humans, Immunoenzyme Techniques, Neovascularization, Pathologic (genetics), Neuroblastoma (blood supply), Neuroblastoma (metabolism), Neuroblastoma (pathology), RNA, Long Noncoding (genetics), RNA, Messenger (genetics), Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Transcriptional Activation.
MESH :
- chemical , genetics : Fibroblast Growth Factor 2, RNA, Long Noncoding, RNA, Messenger.
- chemical , metabolism : Fibroblast Growth Factor 2.
- blood supply : Neuroblastoma.
- cytology : Human Umbilical Vein Endothelial Cells.
- genetics : Neovascularization, Pathologic.
- metabolism : Human Umbilical Vein Endothelial Cells, Neuroblastoma.
- pathology : Neuroblastoma.
- Apoptosis, Blotting, Western, Cell Movement, Cell Proliferation, Cells, Cultured, Enzyme-Linked Immunosorbent Assay, Gene Expression Regulation, Neoplastic, Humans, Immunoenzyme Techniques, Real-Time Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Transcriptional Activation.

Abstract

Neuroblastoma is the most common solid tumor during early childhood. One of the key features of neuroblastoma is extensive tumor-driven angiogenesis due to hypoxia. However, the mechanism through which neuroblastoma cells drive angiogenesis is poorly understood. Here we show that the long noncoding RNA MALAT1 was upregulated in human neuroblastoma cell lines under hypoxic conditions. Conditioned media from neuroblastoma cells transfected with small interfering RNAs (siRNA) targeting MALAT1, compared with conditioned media from neuroblastoma cells transfected with control siRNAs, induced significantly less endothelial cell migration, invasion and vasculature formation. Microarray-based differential gene expression analysis showed that one of the genes most significantly down-regulated following MALAT1 suppression in human neuroblastoma cells under hypoxic conditions was fibroblast growth factor 2 (FGF2). RT-PCR and immunoblot analyses confirmed that MALAT1 suppression reduced FGF2 expression, and Enzyme-Linked Immunosorbent Assays revealed that transfection with MALAT1 siRNAs reduced FGF2 protein secretion from neuroblastoma cells. Importantly, addition of recombinant FGF2 protein to the cell culture media reversed the effects of MALAT1 siRNA on vasculature formation. Taken together, our data suggest that up-regulation of MALAT1 expression in human neuroblastoma cells under hypoxic conditions increases FGF2 expression and promotes vasculature formation, and therefore plays an important role in tumor-driven angiogenesis.

DOI: 10.18632/oncotarget.6675
PubMed: 26848616

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<term>Blotting, Western</term>
<term>Cell Movement</term>
<term>Cell Proliferation</term>
<term>Cells, Cultured</term>
<term>Enzyme-Linked Immunosorbent Assay</term>
<term>Fibroblast Growth Factor 2 (genetics)</term>
<term>Fibroblast Growth Factor 2 (metabolism)</term>
<term>Gene Expression Regulation, Neoplastic</term>
<term>Human Umbilical Vein Endothelial Cells (cytology)</term>
<term>Human Umbilical Vein Endothelial Cells (metabolism)</term>
<term>Humans</term>
<term>Immunoenzyme Techniques</term>
<term>Neovascularization, Pathologic (genetics)</term>
<term>Neuroblastoma (blood supply)</term>
<term>Neuroblastoma (metabolism)</term>
<term>Neuroblastoma (pathology)</term>
<term>RNA, Long Noncoding (genetics)</term>
<term>RNA, Messenger (genetics)</term>
<term>Real-Time Polymerase Chain Reaction</term>
<term>Reverse Transcriptase Polymerase Chain Reaction</term>
<term>Transcriptional Activation</term>
</keywords>
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<term>ARN messager (génétique)</term>
<term>Activation de la transcription</term>
<term>Apoptose</term>
<term>Cellules cultivées</term>
<term>Cellules endothéliales de la veine ombilicale humaine (cytologie)</term>
<term>Cellules endothéliales de la veine ombilicale humaine (métabolisme)</term>
<term>Facteur de croissance fibroblastique de type 2 (génétique)</term>
<term>Facteur de croissance fibroblastique de type 2 (métabolisme)</term>
<term>Humains</term>
<term>Mouvement cellulaire</term>
<term>Neuroblastome ()</term>
<term>Neuroblastome (anatomopathologie)</term>
<term>Neuroblastome (métabolisme)</term>
<term>Néovascularisation pathologique (génétique)</term>
<term>Prolifération cellulaire</term>
<term>RT-PCR</term>
<term>Réaction de polymérisation en chaine en temps réel</term>
<term>Régulation de l'expression des gènes tumoraux</term>
<term>Technique de Western</term>
<term>Techniques immunoenzymatiques</term>
<term>Test ELISA</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Fibroblast Growth Factor 2</term>
<term>RNA, Long Noncoding</term>
<term>RNA, Messenger</term>
</keywords>
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</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Neuroblastome</term>
</keywords>
<keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Neuroblastoma</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules endothéliales de la veine ombilicale humaine</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Human Umbilical Vein Endothelial Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Neovascularization, Pathologic</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN long non codant</term>
<term>ARN messager</term>
<term>Facteur de croissance fibroblastique de type 2</term>
<term>Néovascularisation pathologique</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Human Umbilical Vein Endothelial Cells</term>
<term>Neuroblastoma</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules endothéliales de la veine ombilicale humaine</term>
<term>Facteur de croissance fibroblastique de type 2</term>
<term>Neuroblastome</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neuroblastoma</term>
</keywords>
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<term>Blotting, Western</term>
<term>Cell Movement</term>
<term>Cell Proliferation</term>
<term>Cells, Cultured</term>
<term>Enzyme-Linked Immunosorbent Assay</term>
<term>Gene Expression Regulation, Neoplastic</term>
<term>Humans</term>
<term>Immunoenzyme Techniques</term>
<term>Real-Time Polymerase Chain Reaction</term>
<term>Reverse Transcriptase Polymerase Chain Reaction</term>
<term>Transcriptional Activation</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Activation de la transcription</term>
<term>Apoptose</term>
<term>Cellules cultivées</term>
<term>Humains</term>
<term>Mouvement cellulaire</term>
<term>Neuroblastome</term>
<term>Prolifération cellulaire</term>
<term>RT-PCR</term>
<term>Réaction de polymérisation en chaine en temps réel</term>
<term>Régulation de l'expression des gènes tumoraux</term>
<term>Technique de Western</term>
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<front><div type="abstract" xml:lang="en">Neuroblastoma is the most common solid tumor during early childhood. One of the key features of neuroblastoma is extensive tumor-driven angiogenesis due to hypoxia. However, the mechanism through which neuroblastoma cells drive angiogenesis is poorly understood. Here we show that the long noncoding RNA MALAT1 was upregulated in human neuroblastoma cell lines under hypoxic conditions. Conditioned media from neuroblastoma cells transfected with small interfering RNAs (siRNA) targeting MALAT1, compared with conditioned media from neuroblastoma cells transfected with control siRNAs, induced significantly less endothelial cell migration, invasion and vasculature formation. Microarray-based differential gene expression analysis showed that one of the genes most significantly down-regulated following MALAT1 suppression in human neuroblastoma cells under hypoxic conditions was fibroblast growth factor 2 (FGF2). RT-PCR and immunoblot analyses confirmed that MALAT1 suppression reduced FGF2 expression, and Enzyme-Linked Immunosorbent Assays revealed that transfection with MALAT1 siRNAs reduced FGF2 protein secretion from neuroblastoma cells. Importantly, addition of recombinant FGF2 protein to the cell culture media reversed the effects of MALAT1 siRNA on vasculature formation. Taken together, our data suggest that up-regulation of MALAT1 expression in human neuroblastoma cells under hypoxic conditions increases FGF2 expression and promotes vasculature formation, and therefore plays an important role in tumor-driven angiogenesis.</div>
</front>
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<Month>04</Month>
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<Day>09</Day>
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<Month>Feb</Month>
<Day>23</Day>
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<Title>Oncotarget</Title>
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<ArticleTitle>The long noncoding RNA MALAT1 promotes tumor-driven angiogenesis by up-regulating pro-angiogenic gene expression.</ArticleTitle>
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<Abstract><AbstractText>Neuroblastoma is the most common solid tumor during early childhood. One of the key features of neuroblastoma is extensive tumor-driven angiogenesis due to hypoxia. However, the mechanism through which neuroblastoma cells drive angiogenesis is poorly understood. Here we show that the long noncoding RNA MALAT1 was upregulated in human neuroblastoma cell lines under hypoxic conditions. Conditioned media from neuroblastoma cells transfected with small interfering RNAs (siRNA) targeting MALAT1, compared with conditioned media from neuroblastoma cells transfected with control siRNAs, induced significantly less endothelial cell migration, invasion and vasculature formation. Microarray-based differential gene expression analysis showed that one of the genes most significantly down-regulated following MALAT1 suppression in human neuroblastoma cells under hypoxic conditions was fibroblast growth factor 2 (FGF2). RT-PCR and immunoblot analyses confirmed that MALAT1 suppression reduced FGF2 expression, and Enzyme-Linked Immunosorbent Assays revealed that transfection with MALAT1 siRNAs reduced FGF2 protein secretion from neuroblastoma cells. Importantly, addition of recombinant FGF2 protein to the cell culture media reversed the effects of MALAT1 siRNA on vasculature formation. Taken together, our data suggest that up-regulation of MALAT1 expression in human neuroblastoma cells under hypoxic conditions increases FGF2 expression and promotes vasculature formation, and therefore plays an important role in tumor-driven angiogenesis.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tee</LastName>
<ForeName>Andrew E</ForeName>
<Initials>AE</Initials>
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</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Bing</ForeName>
<Initials>B</Initials>
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<Author ValidYN="Y"><LastName>Song</LastName>
<ForeName>Renhua</ForeName>
<Initials>R</Initials>
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</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Jinyan</ForeName>
<Initials>J</Initials>
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   |texte=   The long noncoding RNA MALAT1 promotes tumor-driven angiogenesis by up-regulating pro-angiogenic gene expression.
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	Serveur d'exploration sur les relations entre la France et l'Australie
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The long noncoding RNA MALAT1 promotes tumor-driven angiogenesis by up-regulating pro-angiogenic gene expression.

The long noncoding RNA MALAT1 promotes tumor-driven angiogenesis by up-regulating pro-angiogenic gene expression.

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