Abstract
TGF-β/Smad2/3 signal pathway is regarded as a central regulator in various tumors, but its roles in brain cancer therapy remain unknown. In this study, we identify that the TGF-β/Smad2/3 signal pathway is activated in human brain glioma cells; inhibitor (SB203580) and siRNA against Smad2/3 quickly inhibited the phosphorylation of Smad2 and 3, expression of its major downstream gene, Ki-67, arrested cells in the G2/M phase and induced apoptosis of cells. The findings suggest that TGF-β/Smad2/3 pathway plays a key role in U251 cell growth and metastasis, which suggests its potential role in the molecular therapy of brain cancer.
Keywords:
Apoptosis; Bcl-2; Caspase-3; TGF-β/Smad2/3.
Copyright © 2015 Elsevier B.V. All rights reserved.
MeSH terms
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Apoptosis / drug effects
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Cell Line, Tumor
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Cell Proliferation / drug effects
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G2 Phase Cell Cycle Checkpoints / drug effects
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Gene Expression Regulation, Neoplastic*
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Humans
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Imidazoles / pharmacology
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Ki-67 Antigen / genetics
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Ki-67 Antigen / metabolism
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Neuroglia / drug effects
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Neuroglia / metabolism
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Neuroglia / pathology
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Phosphorylation / drug effects
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Pyridines / pharmacology
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RNA, Small Interfering / genetics
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RNA, Small Interfering / metabolism
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Signal Transduction / genetics*
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Smad2 Protein / antagonists & inhibitors
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Smad2 Protein / genetics*
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Smad2 Protein / metabolism
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Smad3 Protein / antagonists & inhibitors
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Smad3 Protein / genetics*
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Smad3 Protein / metabolism
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Transforming Growth Factor beta / genetics*
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Transforming Growth Factor beta / metabolism
Substances
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Imidazoles
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Ki-67 Antigen
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Pyridines
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RNA, Small Interfering
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SMAD2 protein, human
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SMAD3 protein, human
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Smad2 Protein
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Smad3 Protein
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Transforming Growth Factor beta
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SB 203580