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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 FcγRII immunoglobulin receptor in mediating retinoic acid-induced growth arrest and differentiation of HL-60 cells is presented. HL-60 cells stably transfected with the Δ205 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. Δ205 transfected cells were compared with parental HL-60 cells by differential display to identify differentially expressed genes, which are regulated downstream of Δ205 and might facilitate cellular response to retinoic acid. Differential display revealed that the FcγRII immunoglobulin receptor was differentially expressed. HL-60 cells express FcγRIIA but not FcγRIIB …