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Insulin-like growth factor-binding protein 2-driven glioma progression is prevented by blocking a clinically significant integrin, integrin-linked kinase, and NF-κB network.

Insulin-like growth factor-binding protein 2 (IGFBP2) is increasingly recognized as a glioma oncogene, emerging as a target for therapeutic intervention. In this study, we used an integrative approach to characterizing the IGFBP2 network, combining transcriptional profiling of human glioma with vali... Full description

Journal Title: Proceedings of the National Academy of Sciences of the United States of America February 28, 2012, Vol.109(9), pp.3475-3480
Main Author: Holmes, Kristen M
Other Authors: Annala, Matti , Chua, Corrine Y X , Dunlap, Sarah M , Liu, Yuexin , Hugen, Niek , Moore, Lynette M , Cogdell, David , Hu, Limei , Nykter, Matti , Hess, Kenneth , Fuller, Gregory N , Zhang, Wei
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1120375109
Link: http://search.proquest.com/docview/925718471/?pq-origsite=primo
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title: Insulin-like growth factor-binding protein 2-driven glioma progression is prevented by blocking a clinically significant integrin, integrin-linked kinase, and NF-κB network.
format: Article
creator:
  • Holmes, Kristen M
  • Annala, Matti
  • Chua, Corrine Y X
  • Dunlap, Sarah M
  • Liu, Yuexin
  • Hugen, Niek
  • Moore, Lynette M
  • Cogdell, David
  • Hu, Limei
  • Nykter, Matti
  • Hess, Kenneth
  • Fuller, Gregory N
  • Zhang, Wei
subjects:
  • Animals–Genetics
  • Astrocytoma–Metabolism
  • Avian Proteins–Genetics
  • Brain Neoplasms–Genetics
  • Cell Line, Tumor–Pathology
  • Disease Progression–Therapy
  • Gene Expression Regulation, Neoplastic–Administration & Dosage
  • Genes, Synthetic–Therapeutic Use
  • Genes, Sis–Genetics
  • Genetic Therapy–Pathology
  • Genetic Vectors–Therapy
  • Glioblastoma–Genetics
  • Humans–Toxicity
  • I-Kappa B Proteins–Biosynthesis
  • Insulin-Like Growth Factor Binding Protein 2–Genetics
  • Integrin Beta1–Physiology
  • Intermediate Filament Proteins–Toxicity
  • Kaplan-Meier Estimate–Physiology
  • Mice–Genetics
  • Mice, Transgenic–Physiology
  • Nf-Kappab Inhibitor Alpha–Biosynthesis
  • Nf-Kappa B–Genetics
  • Neoplasm Invasiveness–Physiology
  • Neoplasm Proteins–Genetics
  • Nerve Tissue Proteins–Genetics
  • Nestin–Metabolism
  • Oligodendroglioma–Physiology
  • Prognosis–Toxicity
  • Protein-Serine-Threonine Kinases–Genetics
  • Receptors, Virus–Physiology
  • Retroviridae–Physiology
  • Signal Transduction–Physiology
  • Avian Proteins
  • I-Kappa B Proteins
  • Insulin-Like Growth Factor Binding Protein 2
  • Integrin Beta1
  • Intermediate Filament Proteins
  • Nes Protein, Human
  • Nf-Kappa B
  • Nfkbia Protein, Human
  • Neoplasm Proteins
  • Nerve Tissue Proteins
  • Nes Protein, Mouse
  • Nestin
  • Nfkbia Protein, Mouse
  • Receptors, Virus
  • Tva Receptor
  • Nf-Kappab Inhibitor Alpha
  • Integrin-Linked Kinase
  • Protein-Serine-Threonine Kinases
ispartof: Proceedings of the National Academy of Sciences of the United States of America, February 28, 2012, Vol.109(9), pp.3475-3480
description: Insulin-like growth factor-binding protein 2 (IGFBP2) is increasingly recognized as a glioma oncogene, emerging as a target for therapeutic intervention. In this study, we used an integrative approach to characterizing the IGFBP2 network, combining transcriptional profiling of human glioma with validation in glial cells and the replication-competent ASLV long terminal repeat with a splice acceptor/tv-a glioma mouse system. We demonstrated that IGFBP2 expression is closely linked to genes in the integrin and integrin-linked kinase (ILK) pathways and that these genes are associated with prognosis. We further showed that IGFBP2 activates integrin [beta]1 and downstream invasion pathways, requires ILK to induce cell motility, and activates NF-[kappa]B. Most significantly, the IGFBP2/integrin/ILK/NF-[kappa]B network functions as a physiologically active signaling pathway in vivo by driving glioma progression; interfering with any point in the pathway markedly inhibits progression. The results of this study reveal a signaling pathway that is both targetable and highly relevant to improving the survival of glioma patients. doi/10.1073/pnas.1120375109
language: eng
source:
identifier: E-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1120375109
fulltext: fulltext
issn:
  • 10916490
  • 1091-6490
url: Link


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titleInsulin-like growth factor-binding protein 2-driven glioma progression is prevented by blocking a clinically significant integrin, integrin-linked kinase, and NF-κB network.
creatorHolmes, Kristen M ; Annala, Matti ; Chua, Corrine Y X ; Dunlap, Sarah M ; Liu, Yuexin ; Hugen, Niek ; Moore, Lynette M ; Cogdell, David ; Hu, Limei ; Nykter, Matti ; Hess, Kenneth ; Fuller, Gregory N ; Zhang, Wei
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identifierE-ISSN: 1091-6490 ; DOI: 10.1073/pnas.1120375109
subjectAnimals–Genetics ; Astrocytoma–Metabolism ; Avian Proteins–Genetics ; Brain Neoplasms–Genetics ; Cell Line, Tumor–Pathology ; Disease Progression–Therapy ; Gene Expression Regulation, Neoplastic–Administration & Dosage ; Genes, Synthetic–Therapeutic Use ; Genes, Sis–Genetics ; Genetic Therapy–Pathology ; Genetic Vectors–Therapy ; Glioblastoma–Genetics ; Humans–Toxicity ; I-Kappa B Proteins–Biosynthesis ; Insulin-Like Growth Factor Binding Protein 2–Genetics ; Integrin Beta1–Physiology ; Intermediate Filament Proteins–Toxicity ; Kaplan-Meier Estimate–Physiology ; Mice–Genetics ; Mice, Transgenic–Physiology ; Nf-Kappab Inhibitor Alpha–Biosynthesis ; Nf-Kappa B–Genetics ; Neoplasm Invasiveness–Physiology ; Neoplasm Proteins–Genetics ; Nerve Tissue Proteins–Genetics ; Nestin–Metabolism ; Oligodendroglioma–Physiology ; Prognosis–Toxicity ; Protein-Serine-Threonine Kinases–Genetics ; Receptors, Virus–Physiology ; Retroviridae–Physiology ; Signal Transduction–Physiology ; Avian Proteins ; I-Kappa B Proteins ; Insulin-Like Growth Factor Binding Protein 2 ; Integrin Beta1 ; Intermediate Filament Proteins ; Nes Protein, Human ; Nf-Kappa B ; Nfkbia Protein, Human ; Neoplasm Proteins ; Nerve Tissue Proteins ; Nes Protein, Mouse ; Nestin ; Nfkbia Protein, Mouse ; Receptors, Virus ; Tva Receptor ; Nf-Kappab Inhibitor Alpha ; Integrin-Linked Kinase ; Protein-Serine-Threonine Kinases
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descriptionInsulin-like growth factor-binding protein 2 (IGFBP2) is increasingly recognized as a glioma oncogene, emerging as a target for therapeutic intervention. In this study, we used an integrative approach to characterizing the IGFBP2 network, combining transcriptional profiling of human glioma with validation in glial cells and the replication-competent ASLV long terminal repeat with a splice acceptor/tv-a glioma mouse system. We demonstrated that IGFBP2 expression is closely linked to genes in the integrin and integrin-linked kinase (ILK) pathways and that these genes are associated with prognosis. We further showed that IGFBP2 activates integrin [beta]1 and downstream invasion pathways, requires ILK to induce cell motility, and activates NF-[kappa]B. Most significantly, the IGFBP2/integrin/ILK/NF-[kappa]B network functions as a physiologically active signaling pathway in vivo by driving glioma progression; interfering with any point in the pathway markedly inhibits progression. The results of this study reveal a signaling pathway that is both targetable and highly relevant to improving the survival of glioma patients. doi/10.1073/pnas.1120375109
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authorHolmes, Kristen M ; Annala, Matti ; Chua, Corrine Y X ; Dunlap, Sarah M ; Liu, Yuexin ; Hugen, Niek ; Moore, Lynette M ; Cogdell, David ; Hu, Limei ; Nykter, Matti ; Hess, Kenneth ; Fuller, Gregory N ; Zhang, Wei
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