Abstract
Here we report the negative correlation of phosphorylation of Smad1 and BMPR-IB expression with the development of human glioma. Western blot analysis showed that expression of both phospho-Smad1/5/8 and BMPR-IB were decreased in malignant glioma tissues compared with normal brain tissues. Kaplan-Meier survival curves revealed that lower expression ratio of phospho-Smad1/5/8 to Smad1 expression significantly correlates with poor patient survival. Transient transfection of BMPR-IB activates Smad1 signaling and induces differentiation and apoptosis of U251 and U87 glioblastoma cells. The effects could be blocked by cotransfection of Smad6. These results might provide new molecular marker and target for glioma diagnosis and therapy.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis
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Astrocytoma / genetics
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Astrocytoma / metabolism*
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Astrocytoma / mortality
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Bone Morphogenetic Protein Receptors, Type I / biosynthesis
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Bone Morphogenetic Protein Receptors, Type I / genetics
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Bone Morphogenetic Protein Receptors, Type I / physiology*
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Brain / metabolism
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Brain Neoplasms / genetics
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Brain Neoplasms / metabolism*
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Brain Neoplasms / mortality
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Cell Line, Tumor
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Depression, Chemical
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Gene Expression Regulation, Neoplastic
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Glioblastoma / genetics
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Glioblastoma / metabolism*
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Glioblastoma / mortality
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Humans
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Kaplan-Meier Estimate
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Neoplasm Proteins / genetics
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Neoplasm Proteins / metabolism*
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Nerve Tissue Proteins / genetics
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Nerve Tissue Proteins / physiology
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Phosphorylation
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Prognosis
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Protein Processing, Post-Translational
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Smad1 Protein / genetics
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Smad1 Protein / metabolism
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Smad1 Protein / physiology*
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Smad5 Protein / metabolism
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Smad8 Protein / metabolism
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Survival Analysis
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Transfection
Substances
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Neoplasm Proteins
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Nerve Tissue Proteins
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SMAD1 protein, human
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SMAD5 protein, human
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SMAD9 protein, human
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Smad1 Protein
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Smad5 Protein
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Smad8 Protein
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Bone Morphogenetic Protein Receptors, Type I