A dual block to cell cycle progression in HL60 cells exposed to analogues of vitamin D,

J. J. Godyn, H. Xu, F. Zhang, S. Kolla, George Studzinski

Research output: Contribution to journalArticle

59 Citations (Scopus)

Abstract

Abstract. The physiologically active form of vitamin D3, 1,25‐dihydroxy‐vitamin D3, (1,25(OH)2, D3), induces differentiation of several types of myeloid leukaemia cells. The acquisition of monocyte‐like phenotype is accompanied by slower progression through the cell cycle, and G1, block has been reported to be the basis of this effect. It is shown here that human promyelocytic leukaemia HL60 cells treated with analogues of vitamin D3, which are potent inducers of monocytic differentiation, have an additional cell cycle block. Exposure to 10‐7m 1,25(OH)2, D3, or 1,25‐(OH)2,‐16‐ene‐D3 resulted in monocytic differentiation and the expected G1, block evident at approximately 48 h in a rapidly differentiating variant of HL60 cells (HL60‐G), and at 96 h in the more slowly differentiating HL60‐240 cells. In addition, a G2,+M block was noted at approximately 72 h in HL60‐G and HL60‐240 cells. Exposure to vitamin D3, analogues also markedly increased the number of dikaryons, suggesting that cytokinesis was impaired more than karyokinesis. Treatment with a third analogue 25‐hydroxy‐16,23‐diene‐D3, produced little differentiation and had minimal effects on the cell cycle parameters. These findings indicate that vitamin D3, analogues regulate cell proliferation by control of the transition of G1, and G2,+M phases, reminiscent of the cdc2/CDK2 type of cell cycle control.

Original languageEnglish (US)
Pages (from-to)37-46
Number of pages10
JournalCell Proliferation
Volume27
Issue number1
DOIs
StatePublished - Jan 1 1994

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Cholecalciferol
HL-60 Cells
Vitamin D
Cell Cycle
Cell Nucleus Division
Myeloid Leukemia
Cytokinesis
G2 Phase
Myeloid Cells
Cell Cycle Checkpoints
Cell Division
Leukemia
Cell Proliferation
Phenotype

All Science Journal Classification (ASJC) codes

  • Cell Biology

Cite this

Godyn, J. J. ; Xu, H. ; Zhang, F. ; Kolla, S. ; Studzinski, George. / A dual block to cell cycle progression in HL60 cells exposed to analogues of vitamin D,. In: Cell Proliferation. 1994 ; Vol. 27, No. 1. pp. 37-46.
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A dual block to cell cycle progression in HL60 cells exposed to analogues of vitamin D, / Godyn, J. J.; Xu, H.; Zhang, F.; Kolla, S.; Studzinski, George.

In: Cell Proliferation, Vol. 27, No. 1, 01.01.1994, p. 37-46.

Research output: Contribution to journalArticle

TY - JOUR

T1 - A dual block to cell cycle progression in HL60 cells exposed to analogues of vitamin D,

AU - Godyn, J. J.

AU - Xu, H.

AU - Zhang, F.

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N2 - Abstract. The physiologically active form of vitamin D3, 1,25‐dihydroxy‐vitamin D3, (1,25(OH)2, D3), induces differentiation of several types of myeloid leukaemia cells. The acquisition of monocyte‐like phenotype is accompanied by slower progression through the cell cycle, and G1, block has been reported to be the basis of this effect. It is shown here that human promyelocytic leukaemia HL60 cells treated with analogues of vitamin D3, which are potent inducers of monocytic differentiation, have an additional cell cycle block. Exposure to 10‐7m 1,25(OH)2, D3, or 1,25‐(OH)2,‐16‐ene‐D3 resulted in monocytic differentiation and the expected G1, block evident at approximately 48 h in a rapidly differentiating variant of HL60 cells (HL60‐G), and at 96 h in the more slowly differentiating HL60‐240 cells. In addition, a G2,+M block was noted at approximately 72 h in HL60‐G and HL60‐240 cells. Exposure to vitamin D3, analogues also markedly increased the number of dikaryons, suggesting that cytokinesis was impaired more than karyokinesis. Treatment with a third analogue 25‐hydroxy‐16,23‐diene‐D3, produced little differentiation and had minimal effects on the cell cycle parameters. These findings indicate that vitamin D3, analogues regulate cell proliferation by control of the transition of G1, and G2,+M phases, reminiscent of the cdc2/CDK2 type of cell cycle control.

AB - Abstract. The physiologically active form of vitamin D3, 1,25‐dihydroxy‐vitamin D3, (1,25(OH)2, D3), induces differentiation of several types of myeloid leukaemia cells. The acquisition of monocyte‐like phenotype is accompanied by slower progression through the cell cycle, and G1, block has been reported to be the basis of this effect. It is shown here that human promyelocytic leukaemia HL60 cells treated with analogues of vitamin D3, which are potent inducers of monocytic differentiation, have an additional cell cycle block. Exposure to 10‐7m 1,25(OH)2, D3, or 1,25‐(OH)2,‐16‐ene‐D3 resulted in monocytic differentiation and the expected G1, block evident at approximately 48 h in a rapidly differentiating variant of HL60 cells (HL60‐G), and at 96 h in the more slowly differentiating HL60‐240 cells. In addition, a G2,+M block was noted at approximately 72 h in HL60‐G and HL60‐240 cells. Exposure to vitamin D3, analogues also markedly increased the number of dikaryons, suggesting that cytokinesis was impaired more than karyokinesis. Treatment with a third analogue 25‐hydroxy‐16,23‐diene‐D3, produced little differentiation and had minimal effects on the cell cycle parameters. These findings indicate that vitamin D3, analogues regulate cell proliferation by control of the transition of G1, and G2,+M phases, reminiscent of the cdc2/CDK2 type of cell cycle control.

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