title: HL60 cells halted in G1 or S phase differentiate normally.
abstract: 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.
authors.affiliation: Division of Immunity & Infection, University of Birmingham, Birmingham B15 2TT, United Kingdom. G.Brown@bham.ac.uk
authors.forename: Geoffrey
authors.initials: G
authors.lastname: Brown
authors.forename: Mark T
authors.initials: MT
authors.lastname: Drayson
authors.forename: Jennifer
authors.initials: J
authors.lastname: Durham
authors.forename: Kai Michael
authors.initials: KM
authors.lastname: Toellner
authors.forename: Philip J
authors.initials: PJ
authors.lastname: Hughes
authors.forename: M Ansar
authors.initials: MA
authors.lastname: Choudhry
authors.forename: Dale R
authors.initials: DR
authors.lastname: Taylor
authors.forename: Roger
authors.initials: R
authors.lastname: Bird
authors.forename: Robert H
authors.initials: RH
authors.lastname: Michell
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology; D039481:CD11b Antigen / Q000378:metabolism; D002454:Cell Differentiation / Q000502:physiology*; D002455:Cell Division / Q000187:drug effects; D017931:DNA Primers / Q000737:chemistry; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005434:Flow Cytometry; D016193:G1 Phase / Q000187:drug effects*; D018922:HL-60 Cells / Q000166:cytology* / Q000378:metabolism; D006801:Humans; D017730:Ki-1 Antigen / Q000378:metabolism; D018950:Lipopolysaccharide Receptors / Q000378:metabolism; D016177:Macrophage-1 Antigen / Q000378:metabolism; D009000:Monocytes / Q000166:cytology* / Q000378:metabolism; D009504:Neutrophils / Q000166:cytology* / Q000378:metabolism; D016186:Receptor, Macrophage Colony-Stimulating Factor / Q000378:metabolism; D016188:Receptors, Granulocyte Colony-Stimulating Factor / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016196:S Phase / Q000187:drug effects*
chemical_list: D000970:Antineoplastic Agents; D039481:CD11b Antigen; D017931:DNA Primers; D004791:Enzyme Inhibitors; D017730:Ki-1 Antigen; D018950:Lipopolysaccharide Receptors; D016177:Macrophage-1 Antigen; D016188:Receptors, Granulocyte Colony-Stimulating Factor; D016186:Receptor, Macrophage Colony-Stimulating Factor