HL60 cells halted in G1 or S phase differentiate normally.
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.
Brown
Geoffrey
G
Division of Immunity & Infection, University of Birmingham, Birmingham B15 2TT, United Kingdom. G.Brown@bham.ac.uk
Drayson
Mark T
MT
Durham
Jennifer
J
Toellner
Kai Michael
KM
Hughes
Philip J
PJ
Choudhry
M Ansar
MA
Taylor
Dale R
DR
Bird
Roger
R
Michell
Robert H
RH
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*
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