C-Myc and Bcl-2 protein expression during the induction of apoptosis and differentiation in TNF alpha-treated HL-60 cells

Leuk Lymphoma. 1996 Oct;23(3-4):383-94. doi: 10.3109/10428199609054843.


We examined c-Myc and Bcl-2 protein expressions during the induction of apoptosis and differentiation in TNF alpha-treated HL-60 cells using a two-color flow cytometric method. We found that c-Myc protein was rapidly down-regulated in the apoptotic cells while Bcl-2 protein was expressed at relatively high levels. Concomitantly with terminal differentiation Bcl-2 protein was down-regulated in differentiating cells as well as c-Myc protein. We also showed that c-myc antisense oligonucleotides could induce apoptosis in HL-60 cells whereas bcl-2 antisense did not induce apoptosis during the early time of treatment. These results suggest that the down-regulation of c-Myc protein expression is a primary event to induce apoptosis and neither consistent expression of c-Myc protein nor rapid down-regulation of Bcl-2 protein is necessary for the initial processing of apoptosis in HL-60 cells. Furthermore, concomitant down-regulation of c-Myc and Bcl-2 is closely associated with terminal differentiation and apoptotic cell death of HL-60 cells treated with TNF alpha.

MeSH terms

  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Cell Differentiation / drug effects
  • Cell Differentiation / physiology
  • DNA, Neoplasm / metabolism
  • Down-Regulation
  • Flow Cytometry
  • HL-60 Cells / cytology*
  • HL-60 Cells / drug effects*
  • HL-60 Cells / metabolism
  • Humans
  • Oligonucleotides, Antisense / pharmacology
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / physiology*
  • Proto-Oncogene Proteins c-myc / metabolism
  • Proto-Oncogene Proteins c-myc / physiology*
  • Tumor Necrosis Factor-alpha / pharmacology*


  • DNA, Neoplasm
  • Oligonucleotides, Antisense
  • Proto-Oncogene Proteins c-bcl-2
  • Proto-Oncogene Proteins c-myc
  • Tumor Necrosis Factor-alpha