Transcription interruption may be a common mechanism of c-myc regulation during HL-60 differentiation.

Human promyelocytic leukemia cells (HL-60) differentiate along a monocytoid pathway in response to recombinant human tumor necrosis factor or recombinant human interferon gamma. Together, these agents act synergistically to induce phenotypic differentiation. Since reduced expression of mRNA for the proto-oncogene c-myc correlates with differentiation of HL-60 cells induced by other agents, we tested the abilities of tumor necrosis factor and interferon gamma to regulate expression of c-myc mRNA.

Dioctanoylglycerol and phorbol esters regulate transcription of c-myc in human promyelocytic leukemia cells.

Treatment of human promyelocytic leukemia cells (HL-60) with phorbol 12-myristate 13-acetate or phorbol 12,13-dibutyrate (PDBu) caused a rapid decrease in transcription of the c-myc protooncogene. In the continuous presence of PMA or PDBu, the rate of transcription of c-myc decreased to 20% of control within 2 h and was maintained at 20-30% of the control level for the ensuing 24 h. Cell-permeable sn-1,2-dioctanoylglycerol (diC8), a diacylglycerol analogue, also caused a rapid decrease in c-myc transcription.