Retinoic acid induced HL-60 myeloid differentiation: Dependence of early and late events on isomeric structure

Yen, Andrew; Powers, Vickie; Fishbaugh, Justin

doi:10.1016/0145-2126(86)90264-x

Cited by 28 publications

(8 citation statements)

References 21 publications

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“…Breitman et al (7,8) demonstrated that retinoic acid inhibits proliferation of HL-60 cells and induces them to differentiate into morphologically functional mature granulocytes. This finding has been substantiated in other laboratories (9)(10)(11)(12)(13)(14). The well-established anticarcinogenic effect of retinoids in experimental systems has suggested a potential for clinical use of retinoids as cancer preventive or chemotherapeutic agents.…”

supporting

confidence: 68%

Induction of differentiation of human promyelocytic leukemia cell line HL-60 by retinoyl glucuronide, a biologically active metabolite of vitamin A.

Zile¹,

Cullum²,

Simpson³

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

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We examined the differentiation activity of retinoyl p-D-glucuronide, a biologically active physiological metabolite of vitamin A, using the human promyelocytic leukemic cell line HL-60, which can be induced to differentiate with retinoic acid. Retinoyl /3-D-glucuronide (1 ,AM) inhibited HL-60 cell proliferation by 55-75%, inhibited tritiated thymidine incorporation into DNA by 63-80%, and induced 38-50% of the cells to differentiate into mature granulocytes. The potency of growth inhibition and induction of differentiation by retinoyl .8-D-glucuronide was similar to that of all-trans-retinoic acid. The continuous presence of either retinoyl .l-Dglucuronide or all-trans-retinoic acid was not required to obtain maximum growth arrest and differentiation: a 1-hr exposure of HL-60 cells to the retinoids gave the same response (measured after a total incubation time of 48 hr) as a 24-hr or 48-hr continuous treatment. Retinoyl j3-D-glucuronide (0.1-0.2 mM) was 50% less cytotoxic to HL-60 cells than all-trans-retinoic acid at an equimolar concentration. Retinoyl P-D-glucuronide was not significantly metabolized to other retinoids; retinoic acid was not formed during incubation. We conclude that retinoyl ,8-D-glucuronide can arrest HL-60 cell proliferation and induce their differentiation into mature granulocytes; it may act by itself or by being hydrolyzed to retinoic acid, which could be immediately utilized and metabolized. The therapeutic use of this retinoid as an antineoplastic agent is suggested.

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supporting

confidence: 68%

Induction of differentiation of human promyelocytic leukemia cell line HL-60 by retinoyl glucuronide, a biologically active metabolite of vitamin A.

Zile¹,

Cullum²,

Simpson³

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

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“…Samples were analyzed by flow cytometry as described previously (15). 2) For NBT assay, the percentage of cells capable of inducible oxidative metabolism, a functional marker for mature myelomonocytic cells, was measured as the percentage of cells capable of reducing NBT to intracellular formazan because of superoxide as described previously (16,17). Cells were harvested and scored by microscopy for formazan.…”

Section: Methodsmentioning

confidence: 99%

A MAPK-positive Feedback Mechanism for BLR1 Signaling Propels Retinoic Acid-triggered Differentiation and Cell Cycle Arrest

Wang

Yen

2008

Journal of Biological Chemistry

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106

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“…The human myeloid leukemic cell line HL-60 (1) is a bipotential cell that can be differentiated by various agents either to the monocytic or granulocytic pathway (2 of differentiation, which are not necessarily coupled (3)(4)(5), and by using clonal assays after exposing cells to dimethylsulfoxide and retinoic acid (6,7). The present study takes a different experimental approach by using whole cell populations in liquid culture as the differentiation target.…”

Section: Introductionmentioning

confidence: 99%

Retinoic Acid Induced Differentiation and Commitment in HL-60 Cells

Meyer¹,

Kleinschnitz²

1990

Environmental Health Perspectives

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Retinoic acid induced HL-60 myeloid differentiation: Dependence of early and late events on isomeric structure

Cited by 28 publications

References 21 publications

Induction of differentiation of human promyelocytic leukemia cell line HL-60 by retinoyl glucuronide, a biologically active metabolite of vitamin A.

Induction of differentiation of human promyelocytic leukemia cell line HL-60 by retinoyl glucuronide, a biologically active metabolite of vitamin A.

A MAPK-positive Feedback Mechanism for BLR1 Signaling Propels Retinoic Acid-triggered Differentiation and Cell Cycle Arrest

Retinoic Acid Induced Differentiation and Commitment in HL-60 Cells

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