Interleukin‐4 inhibits the differentiation of mouse myeloid leukemia M1 cells induced by dexamethasone, D‐factor/leukemia inhibitory factor and interleukin‐6, but not by 1α,25‐dihydroxyvitamin D<sub>3</sub>

Kasukabe, Takashi; Okabe‐Kado, Junko; Honma, Yoshio; Motohashi, Hozumi

doi:10.1016/0014-5793(91)81278-g

Cited by 9 publications

(3 citation statements)

References 23 publications

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“…The possibility of enhancing the effects of VD in vitro by combining the hormone with other molecules such as growth factors or other chemotherapic agents has been explored. Recently the synergistic effect of VD with granulocyte‐macrophage colony‐stimulating factor on the differentiation of the human monocytic cell line U937 has been demonstrated [36] with interferon‐gamma and tumour necrosis factor in inducing the monocytoid differentiation of human promyelocytic cells [37], and with IL4 in enhancing its antiproliferative effect on mouse monocytic leukaemia cells [38]. Another approach is to combine VD with other inducers of differentiation presenting a synergistic effect [39].…”

Section: Discussionmentioning

confidence: 99%

Effects of vitamin D on the growth of normal and malignant B-cell progenitors

Consolini

Pala

Legitimo

et al. 2001

Clinical and Experimental Immunology

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SUMMARYAs the effects of vitamin D 3 , 1,25-dihydroxyvitamin D 3 (1,25-(OH) 2 -D 3 ) (VD, calcitriol) on the proliferation and differentiation potential of normal and leukaemic cells in vitro of myeloid lineage are known, we investigated the response to VD on the growth of both normal and malignant lymphoid progenitors. Effects of vitamin D on normal human lymphoid progenitors and B lineage acute lymphoblastic leukaemia (ALL) progenitors were assessed by using an in vitro cell colony assay specific for either B or T cell lineages. The expression of VDR on B untreated malignant progenitors at diagnosis was investigated by RT-PCR analysis. VD induced a significant inhibition of normal lymphoid cell progenitors growth of both T and B lineage. VD inhibited significantly also the growth of malignant B cell lineage lymphoid progenitors, without inducing cytotoxic effect. As it has been reported that VD effects on activated lymphocytes are mediated by 1,25-(OH) 2 -D 3 nuclear receptor (VDR), we investigated VDR expression on malignant B cell progenitors. We did not detect VDR expression on these cells examined at diagnosis. We demonstrated that VD inhibited in vitro the clonogenic growth of both normal and malignant lymphoid B cell progenitors and that this inhibitory effect on malignant B cell progenitors was not related to VDR. Our work contributes to understanding of the mechanism of action of this hormone in promoting cellular inhibition of clonal growth of malignant lymphoid B cell progenitors, suggesting that the regulation of some critical growth and differentiation factor receptors could be a key physiological role of this hormone.

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Section: Discussionmentioning

confidence: 99%

Effects of vitamin D on the growth of normal and malignant B-cell progenitors

Consolini

Pala

Legitimo

et al. 2001

Clinical and Experimental Immunology

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“…To examine the cellular basis of the restrictive BeAn virus replication in Ms, we used the myeloid precursor cell line M1, derived from a spontaneous myeloid leukemia of SL mice (18,19). M1 cells differentiate in vitro into either M-or granulocyte-like cells in response to conditioned medium from embryonic cell cultures (18,19), various cytokines (33,34) including interleukin-6 (IL-6) (7,16,42), macrophage colony-stimulating factor (M-CSF) (46), and chemicals such as dexamethasone or 1␣,23dihydroxyvitamin D 3 (22). Differentiated M1 cells upregulate several cell surface proteins, including Fc receptors (FcR), (49), tumor necrosis factor alpha receptors (29), and MHC class II proteins, and they acquire functions such as phagocytosis and lysozyme secretion (40).…”

Section: Infection Of Susceptible Mouse Strains With Bean a Less Virmentioning

confidence: 99%

Differentiation of M1 Myeloid Precursor Cells into Macrophages Results in Binding and Infection by Theiler’s Murine Encephalomyelitis Virus and Apoptosis

Jelachich

Bramlage

Lipton

1999

J Virol

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Infection of susceptible mouse strains with BeAn, a less virulent strain of Theiler’s murine encephalomyelitis virus (TMEV), results in immune system-mediated demyelinating lesions in the central nervous system (CNS) similar to those in multiple sclerosis. Since macrophages appear to carry the major detectable antigen burden in vivo, and purification of sufficient cell numbers from the CNS for detailed analysis is difficult, macrophage-like cell lines provide an accessible system with which to study virus-macrophage interactions. The myeloid precursor cell line M1 differentiates in response to cytokines and expresses many characteristics of tissue macrophages. Incubation of TMEV with undifferentiated M1 cells produced neither infection nor apoptosis, whereas differentiated M1 (M1-D) cells developed a restricted virus infection and changes indicative of apoptosis. Virus binding and RNA replication as well as cellular production of alpha/beta interferons increased with differentiation. Although the amount of infectious virus was highly restricted, BeAn-infected M1-D cells synthesized and appropriately processed virus capsid proteins at levels comparable to those for permissive BHK-21 cells. Analysis of Bcl-2 protein family expression in undifferentiated and differentiated cells suggests that susceptibility of M1-D cells to apoptosis may be controlled, in part, by expression of the proapoptotic α isoform of Bax and Bak. These data suggest that macrophage differentiation plays a role in susceptibility to TMEV infection and apoptosis.

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“…Interferon-gamma and 1,25-(OH) 2 D 3 synergistically inhibit the proliferation and stimulate the differentiation of HL-60 and WEHI-3 myelocytic leukemia cells [158,159] and in the mouse myeoloid leukemia cells M1 interleukin-4 enhanced 1,25-(OH) 2 D 3 -induced differentiation [160]. 1,25-(OH) 2 D 3 and tumor necrosis factor synergistically induce growth inhibition and differentiation of HL-60 cells [161].…”

Section: 25-(oh) 2 D 3 and Vitamin D Analogs In Cancer Patientsmentioning

confidence: 99%

Anti-Tumor Effects of 1,25-Dihydroxyvitamin D3 and Vitamin D Analogs

Bemd

Pols²,

Leeuwen³

2000

CPD

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The role of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) as a regulator of cell growth and differentiation is well recognized. Currently, 1, 25-(OH)2D3 and vitamin D analogs are being evaluated for their therapeutic potential in the treatment of hyperproliferative disorders like cancer. In the present review, we will discuss several processes that might be involved in 1,25-(OH)2D3- and vitamin D analog-mediated suppression of cancer cell growth. The effects on tumor cell proliferation, differentiation, apoptosis, angiogenesis, metastases, and parathyroid hormone-related peptide secretion will be highlighted. In addition, combination therapy with other tumor effec tive drugs will be addressed. Furtermore, we will focus on the potential drawbacks and the possible side effects of vitamin D compounds in the treatment of cancer.

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Interleukin‐4 inhibits the differentiation of mouse myeloid leukemia M1 cells induced by dexamethasone, D‐factor/leukemia inhibitory factor and interleukin‐6, but not by 1α,25‐dihydroxyvitamin D₃

Cited by 9 publications

References 23 publications

Effects of vitamin D on the growth of normal and malignant B-cell progenitors

Effects of vitamin D on the growth of normal and malignant B-cell progenitors

Differentiation of M1 Myeloid Precursor Cells into Macrophages Results in Binding and Infection by Theiler’s Murine Encephalomyelitis Virus and Apoptosis

Anti-Tumor Effects of 1,25-Dihydroxyvitamin D3 and Vitamin D Analogs

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Interleukin‐4 inhibits the differentiation of mouse myeloid leukemia M1 cells induced by dexamethasone, D‐factor/leukemia inhibitory factor and interleukin‐6, but not by 1α,25‐dihydroxyvitamin D3

Cited by 9 publications

References 23 publications

Effects of vitamin D on the growth of normal and malignant B-cell progenitors

Effects of vitamin D on the growth of normal and malignant B-cell progenitors

Differentiation of M1 Myeloid Precursor Cells into Macrophages Results in Binding and Infection by Theiler’s Murine Encephalomyelitis Virus and Apoptosis

Anti-Tumor Effects of 1,25-Dihydroxyvitamin D3 and Vitamin D Analogs

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Interleukin‐4 inhibits the differentiation of mouse myeloid leukemia M1 cells induced by dexamethasone, D‐factor/leukemia inhibitory factor and interleukin‐6, but not by 1α,25‐dihydroxyvitamin D₃