Abstract
A cDNA microarray analysis indicated that Semaphorin3B (Sema3B), a gene whose product is involved in axon guidance and axonal repulsion, is inducible by p53. Introduction of exogenous p53 into a glioblastoma cell line lacking wild-type p53 (U373MG) dramatically induced expression of Sema3B mRNA. An electrophoretic mobility shift assay and a reporter assay confirmed that a potential p53 binding site present in the promoter region had p53-dependent transcriptional activity. Expression of endogenous Sema3B was induced in response to genotoxic stresses caused by adriamycin treatment or UV irradiation in a p53-dependent manner. Ectopic expression of Sema3B in p53-defective cells reduced the number of colonies in colony formation assays. These results suggest that Sema3B might play some role in regulating cell growth as a mediator of p53 tumor-suppressor activity.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Base Sequence
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Binding Sites
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Blotting, Northern
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Breast Neoplasms / genetics*
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Breast Neoplasms / metabolism
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Colony-Forming Units Assay
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Consensus Sequence
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DNA Damage
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DNA Primers / chemistry
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Electrophoretic Mobility Shift Assay
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Gene Expression Profiling
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Glioblastoma / genetics*
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Glioblastoma / metabolism
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Humans
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Luciferases / metabolism
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Lung Neoplasms / genetics*
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Lung Neoplasms / metabolism
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Membrane Glycoproteins / genetics*
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Molecular Sequence Data
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Oligonucleotide Array Sequence Analysis
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RNA, Messenger / metabolism
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Semaphorins
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Tumor Cells, Cultured / metabolism
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Tumor Cells, Cultured / radiation effects
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Tumor Suppressor Protein p53 / physiology*
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Ultraviolet Rays
Substances
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DNA Primers
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Membrane Glycoproteins
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RNA, Messenger
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SEMA3B protein, human
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Semaphorins
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Tumor Suppressor Protein p53
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Luciferases