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Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853

Retinoic acid is known to cause the cell cycle arrest and myeloid differentiation of HL-60 myeloblastic leukemia cells. Evidence suggesting the possible involvement of the FcRII immunoglobulin receptor in mediating retinoic acid-induced growth arrest and differentiation of HL-60 cells is presented. HL-60 cells stably transfected with the 205 mutant polyoma middle T antigen, a largely debilitated polyoma middle T antigen, are known to undergo accelerated retinoic acid-induced growth arrest and differentiation compared with parental HL-60 cells. 205 transfected cells were compared with parental HL-60 cells by differential display to identify differentially expressed genes, which are regulated downstream of 205 and might facilitate cellular response to retinoic acid. Differential display revealed that the FcRII immunoglobulin receptor was differentially expressed. HL-60 cells express FcRIIA but not FcRIIB. In parental HL-60 cells, retinoic acid up-regulated FcRII expression, and FcRII membrane protein expression increased concomitantly with retinoic acid-induced cell cycle arrest and differentiation. Ectopic expression of FcRIIa1 in HL-60 cells retarded cellular progression through all phases of the cell cycle. For HL-60 cells stably transfected with FcRIIa1, onset of retinoic acid-induced growth arrest and differentiation occurred in fewer cell cycles than for parental HL-60 cells. Similar results occurred with 1,25-dihydroxy vitamin D₃. Retinoic acid-induced tyrosine phosphorylation of various PAGE-detected protein bands in HL-60 cells was enhanced by cross-linking ectopically expressed FcRIIa1 receptor. The known retinoic acid-induced sustained activation of various mitogen-activated protein kinase signaling molecules, including extracellular signal-regulated kinase 2, src-like kinases, and adapter molecules, may in part reflect induced expression of FcRIIA, which is known to activate a similar ensemble of signaling molecules through its ITAM domain. The data suggest that retinoic acid induces increased FcRIIA expression, which is of functional consequence in eliciting growth arrest and differentiation.

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