Potentiation of retinoid-induced differentiation of HL-60 and U937 cell lines by cytokines

Peck, Richard; Bollag, W.

doi:10.1016/0277-5379(91)90061-h

Cited by 58 publications

(18 citation statements)

References 18 publications

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“…TNF has been shown to synergize with ATRA for proliferation and dierentiation of dierent hematopoietic cells (Trincheiri et al, 1987;Tobler et al, 1987;Peck et al, 1991). In addition, we have shown that ATRA inhibits TNF production by macrophages stimulated by lipopolysaccharide and interferon (IFN)-g (Mehta et al, 1994).…”

Section: Introductionmentioning

confidence: 76%

“…Retinoids modulate the growth and dierentiation of both myeloid and epithelial cells in vitro (Breitmann et al, 1980;Drach et al, 1993;Amos et al, 1989;Abemayor et al, 1989). In combination with various cytokines, ATRA shows a synergistic activity for dierentiation of hematopoietic cells (Hemmi et al, 1987;Trincheiri et al, 1987;Tobler et al, 1987;Peck et al, 1991), but the mechanism by which they synergize is not understood. RA have been shown to modulate the receptors for a number of dierent cytokines (Kilian et al, 1988;Sidell et al, 1988;Falk et al, 1991;Jetten et al, 1980;Winzen et al, 1992;Lotan et al, 1992;Sidell et al, 1991;Zheng et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

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All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-κB, activated protein-1 and apoptosis in human lung cancer cells

Manna

Aggarwal

2000

Oncogene

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Retinoids modulate the growth and dierentiation eects of TNF but the mechanism is not understood. In this study, we investigated the eect of all-trans-retinoic acid (ATRA) on the cell surface expression of TNF receptors and receptor-mediated signaling in various human lung cancer cell lines. ATRA treatment of cells that express wild-type p53 (A549 and H460), or null p53 (H1299), or mutant p53 (H596) increased the number of TNF receptors, as determined by the speci®c binding of 125 Ilabeled TNF to these cells, in a dose-and time-dependent manner. Treatment with 2 mM ATRA for 24 h at 378C produced the maximal increase. Scatchard analysis indicated that the increase induced by ATRA was due to an increase in receptor number and not to an increase in anity. The upmodulation of TNF receptors was also con®rmed by covalent receptor-ligand cross-linking studies. The increase in TNF receptors sensitized H596 cells to TNF-induced activation of NF-kB, AP-1 and apoptosis. A549 cells, however, were completely resistant to TNF-induced activation of NF-kB, AP-1 and apoptosis. Treatment of these cells with as little as 0.5 mM ATRA was eective in converting TNF-resistant cells to TNF-sensitive. Overall our results indicate that ATRA induces the TNF receptors in human lung cancer cells, which sensitizes them to TNF-induced signaling leading to activation of NF-kB, AP-1 and apoptosis.

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Section: Introductionmentioning

confidence: 76%

Section: Introductionmentioning

confidence: 99%

All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-κB, activated protein-1 and apoptosis in human lung cancer cells

Manna

Aggarwal

2000

Oncogene

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“…RA and cytokine combinations, including interferon (IFN), granulocyte colony-stimulating factor (G-CSF), interleukin (IL)-1a, IL-4, tumor necrosis factor (TNF), were found to increase dierentiation of HL60 and U937 cells though these cytokines had no dierentiating eect by themselves (Peck and Bollag, 1991;Nason-Burchenal et al, 1996). Lack of TNFa expression or the expression of IL-3, Gor GM-CSF by blasts from APL patients signi®cantly reduced the dierentiating potential of RA in APL cells (Dubois et al, 1994).…”

Section: Ra and Cytokine Associations For Apl Treatmentmentioning

confidence: 99%

In vivo analysis of the molecular pathogenesis of acute promyelocytic leukemia in the mouse and its therapeutic implications

Merghoub

Pandolfi

1999

Oncogene

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“…Subsequently, many effects of IL-4 on various hematologlcal cell types have been reported enhances granulocyte colony formation by hematopoletic progemtors m the presence of granulocyte colonystlmulatmg factor (G-CSF), but Inhibits macrophage colony formatlon supported by mterleukm-3 (IL-3) and macrophage colony-stlmulatmg factor (M-CSF) [6,7] Peck and Bollag [8] reported that IL-4 slightly enhanced retmold-induced dlfferentlatlon of human promyelocytic leukemia I-IL-60 cells, but the effects of IL-4 on the growths and differentiations of other myelold leukemia cells have scarcely been mvestlgated Mouse myelold lcukemla Ml cells [9] can be induced to differentrate mto macrophage-hke cells by various substances including dexamethasone (Dex) [IO], D-factor/Leukemla lnhlbitory factor (D-factor/LIF)…”

Section: Introductionmentioning

confidence: 99%

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

et al. 1991

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The cfr,crs of mterleukm-4(11-L) on the growth and dlffeeentlatlon of mouse myeloid leukcmla M 1 cells induced by various chfferentlahon mduccrs were investlgdted IL-4 alone did not have any srgnlficant effect on the growth or dlffereatlatlon of MI cells, but InhIbIted thclr dlffcrentlatlon Induced by dexamethasone, D-factor/leukemia mhtbltory factor, or mterleukm 6 IL-4 also restored the prohfceatlon of Ml cells after growth mhtbltion durmg thclr mductlon of dlfferentlatlon by Inducers In contrast, IL-4 enhanced mhtbltlon of growth and mductlon of dlfferentlatlon of Ml cells by la,25-dlhydroxyvltamm Dj These results mdlcate that modulation of dlfferentlatIon of Ml cells by IL-4 depends on the dlfferentlatton InducerInteeleukm-4, Dlfferentlatlon, Geowth, Myelmd leukemia cell, Ml cell

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Potentiation of retinoid-induced differentiation of HL-60 and U937 cell lines by cytokines

Cited by 58 publications

References 18 publications

All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-κB, activated protein-1 and apoptosis in human lung cancer cells

All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-κB, activated protein-1 and apoptosis in human lung cancer cells

In vivo analysis of the molecular pathogenesis of acute promyelocytic leukemia in the mouse and its therapeutic implications

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

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Potentiation of retinoid-induced differentiation of HL-60 and U937 cell lines by cytokines

Cited by 58 publications

References 18 publications

All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-κB, activated protein-1 and apoptosis in human lung cancer cells

All-trans-retinoic acid upregulates TNF receptors and potentiates TNF-induced activation of nuclear factors-κB, activated protein-1 and apoptosis in human lung cancer cells

In vivo analysis of the molecular pathogenesis of acute promyelocytic leukemia in the mouse and its therapeutic implications

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

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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