Retinoic acid-induced granulocytic differentiation of HL-60 myeloid leukemia cells is mediated directly through the retinoic acid receptor (RAR-α)

Steven J. Collins, Kent Robertson, LeMoyne Mueller

Research output: Contribution to journalArticle

279 Citations (Scopus)

Abstract

Retinoic acid (RA) induces terminal granulocytic differentiation of the HL-60 promyelocytic leukemia cell line as well as certain other human myeloid leukemias. Specific RA receptors that are members of the steroid-thyroid hormone superfamily of nuclear transcription factors have recently been identified. We developed an HL-60 subclone that was relatively resistant to RA-induced differentiation. Specific nuclear RA receptors in this RA-resistant subclone had a decreased affinity for RA and exhibited a lower molecular weight compared with nuclear RA receptors from the RA-sensitive parental HL-60 cells. Retroviral vector-mediated transduction of a single copy of the RA receptor (RAR-α) into this RA-resistant HL-60 subclone restored the sensitivity of these cells to RA. These observations indicate that RAR-α plays a critical and central role in mediating RA-induced terminal differentiation of HL-60 leukemia cells.

Original languageEnglish (US)
Pages (from-to)2154-2163
Number of pages10
JournalMolecular and Cellular Biology
Volume10
Issue number5
StatePublished - 1990
Externally publishedYes

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Retinoic Acid Receptors
Myeloid Leukemia
HL-60 Cells
Myeloid Cells
Tretinoin
Leukemia
Thyroid Hormones
Transcription Factors
Molecular Weight
Steroids
Cell Line

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cell Biology

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Retinoic acid-induced granulocytic differentiation of HL-60 myeloid leukemia cells is mediated directly through the retinoic acid receptor (RAR-α). / Collins, Steven J.; Robertson, Kent; Mueller, LeMoyne.

In: Molecular and Cellular Biology, Vol. 10, No. 5, 1990, p. 2154-2163.

Research output: Contribution to journalArticle

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abstract = "Retinoic acid (RA) induces terminal granulocytic differentiation of the HL-60 promyelocytic leukemia cell line as well as certain other human myeloid leukemias. Specific RA receptors that are members of the steroid-thyroid hormone superfamily of nuclear transcription factors have recently been identified. We developed an HL-60 subclone that was relatively resistant to RA-induced differentiation. Specific nuclear RA receptors in this RA-resistant subclone had a decreased affinity for RA and exhibited a lower molecular weight compared with nuclear RA receptors from the RA-sensitive parental HL-60 cells. Retroviral vector-mediated transduction of a single copy of the RA receptor (RAR-α) into this RA-resistant HL-60 subclone restored the sensitivity of these cells to RA. These observations indicate that RAR-α plays a critical and central role in mediating RA-induced terminal differentiation of HL-60 leukemia cells.",
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