Abstract
The B-myb gene is expressed in many cell types at the G1/S transition of the cell cycle. Inhibition of B-myb expression in BALB/c 3T3 fibroblasts by introduction of a B-myb antisense construct greatly diminished cell proliferation, whereas constitutive expression of a human B-myb cDNA in these cells reduced their growth factor requirements and induced a transformed phenotype. Constitutive expression of B-myb cDNA was accompanied by activation of cyclin D1 and cdc2 expression but not of cyclin A and cyclin B. Transfection of BALB/B-myb cells (a cell line expressing high levels of exogenous human B-myb) with a cyclin D1 antisense construct drastically reduced cloning efficiency of these cells. These results suggest that the B-myb-encoded product regulates fibroblast proliferation by activating cdc2 and cyclin D1 gene expression and that abnormal expression of cyclin D1 might be a step in the process of transformation.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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3T3 Cells
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Animals
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Base Sequence
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CDC2 Protein Kinase / biosynthesis*
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CDC2 Protein Kinase / genetics
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CDC2 Protein Kinase / isolation & purification
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Cell Division*
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Cloning, Molecular
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Cyclins / biosynthesis*
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Cyclins / genetics
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Cyclins / isolation & purification
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DNA, Neoplasm / genetics
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Gene Expression
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Humans
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Kinetics
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Mice
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Mice, Inbred BALB C
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Molecular Sequence Data
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Oligodeoxyribonucleotides
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Oligonucleotides, Antisense
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Oncogene Proteins v-myb
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Oncogenes*
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Polymerase Chain Reaction / methods
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Protein-Tyrosine Kinases / genetics*
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RNA, Messenger / isolation & purification
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RNA, Messenger / metabolism
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Retroviridae Proteins, Oncogenic / genetics*
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Transfection
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Tumor Cells, Cultured
Substances
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Cyclins
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DNA, Neoplasm
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Oligodeoxyribonucleotides
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Oligonucleotides, Antisense
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Oncogene Proteins v-myb
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RNA, Messenger
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Retroviridae Proteins, Oncogenic
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Protein-Tyrosine Kinases
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CDC2 Protein Kinase