Interferons induce normal and aberrant retinoic-acid receptors type α in acute promyelocytic leukemia cells: Potentiation of the induction of retinoid-dependent differentiation markers

Giannı̀, Maurizio; Zanotta, Stefania; Terao, Mineko; Garattini, Enrico

doi:10.1002/(sici)1097-0215(19960927)68:1<75::aid-ijc14>3.0.co;2-5

Cited by 25 publications

(10 citation statements)

References 18 publications

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“…G-CSF and IFNs were reported to potentiate differentiation of AML cells. 42,43 Like GM-CSF, the two cytokines signal through the Jak/Stat pathway 44 that could be augmented by SS. 25 The existence of such potential interactions is being examined in our ongoing studies.…”

Section: Discussionmentioning

confidence: 99%

Effects of sodium stibogluconate on differentiation and proliferation of human myeloid leukemia cell lines in vitro

Pathak

2002

Leukemia

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PTPases are key signaling molecules and targets for developing novel therapeutics. We have studied the in vitro biological activity of PTPase inhibitor sodium stibogluconate (SS) on differentiation and proliferation of myeloid leukemia cell lines (NB4, HL-60 and U937). SS (250 g/ml, 6 days) induced 87% of NB4 cells to reduce nitroblue tetrazolium (NBT), in comparison to the 90% induced by ATRA (1 M, 6 days). SS treatment of NB4 cells resulted in an increase of CD11b expression and of a morphologically more mature population, coincident with growth arrest at S phase and increased cell death. The effect of SS on NB4 differentiation was irreversible and required continuous drug exposure. SS (400 g/ml, 6 days) induced 60% and 55% of NBT-positive cells in HL-60 and U937 cell lines, which were augmented in the presence of GM-CSF (25 ng/ml) to levels (85% and 81%, respectively) comparable to those induced by ATRA. SS induced increased tyrosine phosphorylation of cellular proteins in the AML cell lines and inactivated SHP-1 PTPase in NB4 cells, consistent with SS functioning as a PTPase inhibitor in the leukemia cells. These results provide the first evidence of an anti-leukemia activity of SS as a PTPase inhibitor.

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Section: Discussionmentioning

confidence: 99%

Effects of sodium stibogluconate on differentiation and proliferation of human myeloid leukemia cell lines in vitro

Pathak

2002

Leukemia

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“…Analogs of cAMP (8 -12), interferons (13)(14)(15), granulocyte colony-stimulating factor (16), and a novel class of experimental compounds, bis-indols (17), enhance the cytodifferentiating activity of ATRA in AML cell lines. Enhanced cytodifferentia-tion by combinations of bis-indols and ATRA translates into a therapeutically significant effect, as assessed in animal models of APL (17).…”

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Phosphodiesterase IV Inhibition by Piclamilast Potentiates the Cytodifferentiating Action of Retinoids in Myeloid Leukemia Cells

Parrella

Giannı̀

Cecconi

et al. 2004

Journal of Biological Chemistry

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“…33,34 It has been shown that IFNs induce retinoic acid receptors in acute promyelocytic leukemia cells and cooperate with RA to overcome the resistance of cells to RA. 36,52 Also RA activates interferon regulatory factor-1 gene expression in promyelocytic leukemia cells. 53 Our results suggest that IFNs together with RA potentiate the effect of RA on uPA and uPAR production and plasmin formation.…”

Section: Discussionmentioning

confidence: 99%

Interferons and retinoids enhance and dexamethasone suppresses urokinase-mediated plasminogen activation in promyelocytic leukemia cells

et al. 1998

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All-trans retinoic acid (RA) has been successfully used in the treatment of patients with acute promyelocytic leukemia (APL). It induces differentiation of APL cells and reduces the bleeding tendency in APL patients. It has been proposed that plasminogen activation could affect the fibrinolytic balance in patients with leukemia. In our earlier study we found that treatment of APL cells with RA results in changes in urokinase (uPA) production. As interferons (IFNs) and dexamethasone can be used together with RA in the treatment of patients with APL, we have now studied the effects of RA together with IFNs and dexamethasone on the plasminogen activation cascade of these cells, including measurement of plasmin generation and uPA receptor (uPAR), using enzyme immunoassays, fluorescence-activated cell sorter analysis and RNA extraction with Northern blotting. Our main results were: (1) plasmin was formed on the surface of APL cells; (2) RA stimulated transiently plasmin generation and increased uPAR mRNA level; (3) IFNs ␣ and ␥ potentiated RA in its effects on uPA and plasmin activities and on uPAR level; (4) dexamethasone suppressed totally the effect of RA on uPA induction and plasminogen activation; and (5) IFNs and dexamethasone alone did not have potent effects on plasminogen activation. These results may assist in the design of therapy for APL patients.

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Interferons induce normal and aberrant retinoic-acid receptors type α in acute promyelocytic leukemia cells: Potentiation of the induction of retinoid-dependent differentiation markers

Abstract: Q 1996 Wiley-Liss, Inc.

Cited by 25 publications

References 18 publications

Effects of sodium stibogluconate on differentiation and proliferation of human myeloid leukemia cell lines in vitro

Effects of sodium stibogluconate on differentiation and proliferation of human myeloid leukemia cell lines in vitro

Phosphodiesterase IV Inhibition by Piclamilast Potentiates the Cytodifferentiating Action of Retinoids in Myeloid Leukemia Cells

Interferons and retinoids enhance and dexamethasone suppresses urokinase-mediated plasminogen activation in promyelocytic leukemia cells

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