Ectopic expression of cyclin D1 impairs the proliferation and enhances the apoptosis of a murine lymphoid cell line

Cell Death Differ. 2001 Jan;8(1):51-62. doi: 10.1038/sj.cdd.4400768.

Abstract

Cyclin D1, a key regulator of the cell cycle, acts as an oncogene when over-expressed in several types of cancer. In some B-chronic lymphoproliferative disorders, the over-expression of cyclin D1 protein is thought to confer a proliferative phenotype. We have generated BaF3 pro-B cell derivatives in which cyclin D1 can be induced rapidly and reversibly in a dose-dependent manner by the hormone muristerone A. When non-expressing clones displayed the same proliferative capacity as the parental cell line, in the sub-clones, a moderate induction of cyclin D1 lengthened the proliferation rate. The over-expression of cyclin D1 had the same effects on cell proliferation but also led ultimately to cell death by apoptosis. The induction of cyclin D1 in growth factor-deprived cells as well as in anticancer drug-treated cells also reinforced the magnitude of apoptosis. Thus, the expression of cyclin D1 in lymphoid cells does not confer a proliferative advantage but rather alters the response of cells towards apoptotic stimuli in a p53-independent manner.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / drug effects*
  • B-Lymphocytes / cytology
  • B-Lymphocytes / metabolism*
  • Cell Cycle / drug effects
  • Cell Cycle Proteins / metabolism
  • Cell Division / drug effects
  • Cell Line
  • Cell Survival / drug effects
  • Clone Cells
  • Cyclin D1 / biosynthesis*
  • Cyclin D1 / genetics
  • Cyclin D1 / pharmacology
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins / metabolism
  • Dose-Response Relationship, Drug
  • Ecdysterone / analogs & derivatives*
  • Ecdysterone / pharmacology
  • Etoposide / pharmacology
  • Genetic Vectors / genetics
  • Genetic Vectors / metabolism
  • Interleukin-3 / pharmacology
  • Mice
  • Nucleic Acid Synthesis Inhibitors / pharmacology
  • Promoter Regions, Genetic / drug effects
  • Promoter Regions, Genetic / genetics
  • Proto-Oncogene Proteins / metabolism
  • Proto-Oncogene Proteins c-bcl-2*
  • Stem Cells / cytology
  • Stem Cells / metabolism*
  • Transfection
  • Tumor Suppressor Protein p53 / metabolism
  • bcl-2-Associated X Protein

Substances

  • Cdkn1a protein, mouse
  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • Interleukin-3
  • Nucleic Acid Synthesis Inhibitors
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Suppressor Protein p53
  • bcl-2-Associated X Protein
  • Cyclin D1
  • muristerone A
  • Ecdysterone
  • Etoposide