Increased c-myc RNA levels associated with the precommitment state during HL-60 myeloid differentiation.
The dynamics in levels of HL-60 (a human promyelocytic leukemia cell line) c-myc RNA due to retinoic acid-induced myeloid differentiation were measured. An increase in levels of c-myc RNA occurred early in this process when the cells are known to be in a precommitment early regulatory state. The increased levels of c-myc RNA occurred before any G1-0-specific growth arrest or phenotypic differentiation. Cells in G1 and S had similar levels of c-myc RNA during this process. Onset of growth arrest and phenotypic differentiation preceded an apparent decline of c-myc RNA levels. Levels of c-myc RNA decreased only in advanced cultures with growth arrest and differentiation essentially completed. The kinetics and cell cycle dependence of the early increase in c-myc levels paralleled previously reported nuclear structural changes characteristic of the precommitment state. Since c-myc encodes a putative nuclear matrix protein, the results suggest a regulatory role for increased c-myc expression in mediating the nuclear structural change characteristic of precommitment early in the retinoic acid-induced process of HL-60 terminal myeloid differentiation. The results argue against a change in c-myc RNA levels as a requirement for G1 to S transit or for G1-0-specific growth arrest during terminal differentiation. In contrast, the results argue for a putative regulatory role for c-myc in induction of the precommitment early regulatory state. C-myc may thus act in a homeotic regulatory capacity during HL-60 terminal myeloid differentiation.
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D002453:Cell Cycle; D002454:Cell Differentiation / Q000187:drug effects; D002460:Cell Line; D006801:Humans; D015470:Leukemia, Myeloid, Acute / Q000235:genetics* / Q000473:pathology; D011519:Proto-Oncogenes; D012334:RNA, Neoplasm / Q000032:analysis*; D014212:Tretinoin / Q000494:pharmacology
D012334:RNA, Neoplasm; D014212:Tretinoin