HL60 cells halted in G1 or S phase differentiate normally

Exp Cell Res. 2002 Nov 15;281(1):28-38. doi: 10.1006/excr.2002.5654.


Differentiating agents regulate the proliferation and myeloid maturation of HL60 cells by mechanisms that are at least partly independent (Drayson et al., (2001), Exp. Cell Res. 266, 126-134). We have investigated whether halting HL60 cells in G1 or S phase influences their commitment to or maturation along the neutrophil and monocyte pathways. Early G1 and S phase cells were isolated separately by elutriation. Quinidine was used to block the cell cycle progression of G1 cells and aphidicolin to greatly retard the progression of S phase cells. Neutrophilic (in response to all-trans-retinoic acid) or monocytic (to 1 alpha,25-dihydroxyvitamin D(3)) differentiation were assessed by induction of CD11b, M-CSF receptor and CD14 expression, acquisition of granulocyte-colony stimulating factor responsiveness, capacities to phagocytose yeast and reduce nitroblue tetrazolium, and down-regulation of CD30 and transferrin receptor expression. The cell-cycle-blocked cells differentiated at normal rates, mostly without incorporating bromodeoxyuridine. These observations establish: (a) that neither transit through the cell cycle nor a cell's position in the cell cycle substantially influences execution of the neutrophilic and monocytic differentiation programs by HL60 cells; and (b) that individual HL60 cells are genuinely bipotent.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology
  • CD11b Antigen / metabolism
  • Cell Differentiation / physiology*
  • Cell Division / drug effects
  • DNA Primers / chemistry
  • Enzyme Inhibitors / pharmacology
  • Flow Cytometry
  • G1 Phase / drug effects*
  • HL-60 Cells / cytology*
  • HL-60 Cells / metabolism
  • Humans
  • Ki-1 Antigen / metabolism
  • Lipopolysaccharide Receptors / metabolism
  • Macrophage-1 Antigen / metabolism
  • Monocytes / cytology*
  • Monocytes / metabolism
  • Neutrophils / cytology*
  • Neutrophils / metabolism
  • Receptor, Macrophage Colony-Stimulating Factor / metabolism
  • Receptors, Granulocyte Colony-Stimulating Factor / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • S Phase / drug effects*


  • Antineoplastic Agents
  • CD11b Antigen
  • DNA Primers
  • Enzyme Inhibitors
  • Ki-1 Antigen
  • Lipopolysaccharide Receptors
  • Macrophage-1 Antigen
  • Receptors, Granulocyte Colony-Stimulating Factor
  • Receptor, Macrophage Colony-Stimulating Factor