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Effects of TPA, bryostatin 1, and retinoic acid on PO‐B, AP‐1, and AP‐2 DNA binding during HL‐60 differentiation

PO‐B was originally characterized as a transcriptional regulatory factor of the pro‐opiomelanocortin (POMC) gene; however, it has become increasingly clear that this protein may be active in tissues outside the pituitary, since it is present in diverse cell types, including differentiated HL‐60 promyelocytic leukemia cells. We previously showed that PO‐B DNA‐binding is progressively induced during differentiation of promyelomonocytic leukemia HL‐60 cells to the macrophage‐like lineage (with phorbol esters). We now report that PO‐B DNA‐binding in HL‐60 cells is similarly induced during differentiation to the granulocytic lineage (with either retinoic acid or dimethylsulfoxide). Either a genetic or pharmacologic blockade of HL‐60 differentiation prohibited these inductive effects. These studies have prompted our interest in the dynamics of other transcription factor changes during HL‐60 differentiation. Of these, we observed that another transcription factor (AP‐1) is also robustly induced at the DNA‐binding level during macrophagelike HL‐60 differentiation, but not during granulocytic differentiation. Conversely, the DNA‐binding of the transcription factor AP‐2 was slightly reduced by TPA‐induced HL‐60 differentiation but unchanged during granulocyte differentiation. From these data, we conclude that the induction of PO‐B DNA binding is a general marker of HL‐60 myelomonocytic differentiation, but that qualitative aspects of the induction of additional distinct transcription factors, such as AP‐L may contribute to lineage‐specific determinants of cell fate. J. Cell. Biochem. 65:308–324. © 1997 Wiley‐Liss, Inc.