HL60 cells halted in G1 or S phase differentiate normally

Geoffrey Brown, Mark Drayson, Jennifer Durham, Kai-Michael Toellner, Philip Hughes, MA Choudhry, Roger Bird, Robert Michell

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28 Citations (Scopus)


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.
Original languageEnglish
Pages (from-to)28-38
Number of pages11
JournalExperimental Cell Research
Issue number1
Publication statusPublished - 15 Nov 2002


  • HL60
  • aphidicolin
  • differentiation
  • myeloid
  • cell cycle
  • quinidine


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