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.
MeSH Terms
3T3 Cells
Animals
Base Sequence
CDC2 Protein Kinase/biosynthesis,genetics,isolation & purification
Cell Division
Cloning, Molecular
Cyclins/biosynthesis,genetics,isolation & purification
DNA, Neoplasm/genetics
Gene Expression
Humans
Kinetics
Mice
Mice, Inbred BALB C
Molecular Sequence Data
Oligodeoxyribonucleotides
Oligonucleotides, Antisense
Oncogene Proteins v-myb
Oncogenes
Polymerase Chain Reaction/methods
Protein-Tyrosine Kinases/genetics
RNA, Messenger/isolation & purification,metabolism
Retroviridae Proteins, Oncogenic/genetics
Transfection
Tumor Cells, Cultured
Chemicals
Cyclins
DNA, Neoplasm
Oligodeoxyribonucleotides
Oligonucleotides, Antisense
Oncogene Proteins v-myb
RNA, Messenger
Retroviridae Proteins, Oncogenic
Protein-Tyrosine Kinases
CDC2 Protein Kinase
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Sala A
Jefferson Cancer Institute, Thomas Jefferson University, Philadelphia, PA 19107.
Calabretta B
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