Inhibition of PDE3, PDE4 and PDE7 potentiates glucocorticoid-induced apoptosis and overcomes glucocorticoid resistance in CEM T leukemic cells
This paper concerns the targeting of cyclic nucleotide phosphodiesterases (PDEs) to induce apoptosis and overcome glucocorticoid resistance of leukemic cells. Stimulation of the cAMP signaling pathway has been shown to induce apoptosis and augment the effects of glucocorticoids in inducing apoptosis...
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Published in | Biochemical pharmacology Vol. 79; no. 3; pp. 321 - 329 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
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01.02.2010
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Abstract | This paper concerns the targeting of cyclic nucleotide phosphodiesterases (PDEs) to induce apoptosis and overcome glucocorticoid resistance of leukemic cells.
Stimulation of the cAMP signaling pathway has been shown to induce apoptosis and augment the effects of glucocorticoids in inducing apoptosis in leukemic cells. We recently reported that in primary B cell chronic lymphocytic leukemic (B-CLL) cells, apoptosis could be induced by stimulating the cAMP signaling pathway with a phosphodiesterase4 (PDE4) inhibitor alone; while in contrast, in the CEM T leukemic cell line, PDE4 inhibitors alone were ineffective, and concurrent stimulation of adenylyl cyclase was required to see effects [Tiwari et al. (2005) [3]]. We report here that in the CEM and Jurkat T leukemic cell lines, the most abundantly expressed PDEs are PDE3B, PDE4A, PDE4D, PDE7A, and PDE8A. Selective inhibition of PDE3, PDE4 or PDE7 alone produces little effect on cell viability, but inhibition of all three of these PDEs together dramatically enhances glucocorticoid-induced apoptosis in CEM cells, and overcomes glucocorticoid resistance in a glucocorticoid-resistant CEM cell line. These studies indicate that for some leukemic cell types, a desired therapeutic effect may be achieved by inhibiting more than one form of PDE. |
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AbstractList | Stimulation of the cAMP signaling pathway has been shown to induce apoptosis and augment the effects of glucocorticoids in inducing apoptosis in leukemic cells. We recently reported that in primary B cell chronic lymphocytic leukemic (B-CLL) cells, apoptosis could be induced by stimulating the cAMP signaling pathway with a phosphodiesterase4 (PDE4) inhibitor alone; while in contrast, in the CEM T leukemic cell line, PDE4 inhibitors alone were ineffective, and concurrent stimulation of adenylyl cyclase was required to see effects [Tiwari et al. (2005)]. We report here that in the CEM and Jurkat T leukemic cell lines, the most abundantly expressed PDEs are PDE3B, PDE4A, PDE4D, PDE7A, and PDE8A. Selective inhibition of PDE3, PDE4 or PDE7 alone produces little effect on cell viability, but inhibition of all three of these PDEs together dramatically enhances glucocorticoid-induced apoptosis in CEM cells, and overcomes glucocorticoid resistance in a glucocorticoid-resistant CEM cell line. These studies indicate that for some leukemic cell types, a desired therapeutic effect may be achieved by inhibiting more than one form of PDE. This paper concerns the targeting of cyclic nucleotide phosphodiesterases (PDEs) to induce apoptosis and overcome glucocorticoid resistance of leukemic cells. Stimulation of the cAMP signaling pathway has been shown to induce apoptosis and augment the effects of glucocorticoids in inducing apoptosis in leukemic cells. We recently reported that in primary B cell chronic lymphocytic leukemic (B-CLL) cells, apoptosis could be induced by stimulating the cAMP signaling pathway with a phosphodiesterase4 (PDE4) inhibitor alone; while in contrast, in the CEM T leukemic cell line, PDE4 inhibitors alone were ineffective, and concurrent stimulation of adenylyl cyclase was required to see effects [Tiwari et al. (2005) [3]]. We report here that in the CEM and Jurkat T leukemic cell lines, the most abundantly expressed PDEs are PDE3B, PDE4A, PDE4D, PDE7A, and PDE8A. Selective inhibition of PDE3, PDE4 or PDE7 alone produces little effect on cell viability, but inhibition of all three of these PDEs together dramatically enhances glucocorticoid-induced apoptosis in CEM cells, and overcomes glucocorticoid resistance in a glucocorticoid-resistant CEM cell line. These studies indicate that for some leukemic cell types, a desired therapeutic effect may be achieved by inhibiting more than one form of PDE. Stimulation of the cAMP signaling pathway has been shown to induce apoptosis and augment the effects of glucocorticoids in inducing apoptosis in leukemic cells. We recently reported that in primary B cell chronic lymphocytic leukemic (B-CLL) cells, apoptosis could be induced by stimulating the cAMP signaling pathway with a phosphodiesterase4 (PDE4) inhibitor alone; while in contrast, in the CEM T leukemic cell line, PDE4 inhibitors alone were ineffective, and concurrent stimulation of adenylyl cyclase was required to see effects [Tiwari et al. (2005) [3]]. We report here that in the CEM and Jurkat T leukemic cell lines, the most abundantly expressed PDEs are PDE3B, PDE4A, PDE4D, PDE7A, and PDE8A. Selective inhibition of PDE3, PDE4 or PDE7 alone produces little effect on cell viability, but inhibition of all three of these PDEs together dramatically enhances glucocorticoid-induced apoptosis in CEM cells, and overcomes glucocorticoid resistance in a glucocorticoid-resistant CEM cell line. These studies indicate that for some leukemic cell types, a desired therapeutic effect may be achieved by inhibiting more than one form of PDE. |
Author | Auriga, Cornelia Epstein, Paul M. Hatzelmann, Armin Dong, Hongli Zitt, Christof |
Author_xml | – sequence: 1 givenname: Hongli surname: Dong fullname: Dong, Hongli organization: Signal Transduction Laboratory, Department of Cell Biology, University of Connecticut Health Center, 263 Farmington Ave., Farmington, CT 06030-6125, USA – sequence: 2 givenname: Christof surname: Zitt fullname: Zitt, Christof organization: Discovery Department, Nycomed GmbH, D-78467 Konstanz, Germany – sequence: 3 givenname: Cornelia surname: Auriga fullname: Auriga, Cornelia organization: Discovery Department, Nycomed GmbH, D-78467 Konstanz, Germany – sequence: 4 givenname: Armin surname: Hatzelmann fullname: Hatzelmann, Armin organization: Discovery Department, Nycomed GmbH, D-78467 Konstanz, Germany – sequence: 5 givenname: Paul M. surname: Epstein fullname: Epstein, Paul M. email: Epstein@nso1.uchc.edu organization: Signal Transduction Laboratory, Department of Cell Biology, University of Connecticut Health Center, 263 Farmington Ave., Farmington, CT 06030-6125, USA |
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Keywords | Glucocorticoids cAMP Leukemia Phosphodiesterase Cyclic AMP Malignant hemopathy Glucocorticoid Resistance Cell death T-Lymphocyte AMP-3',5' Inhibitor Cancer Apoptosis |
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Snippet | This paper concerns the targeting of cyclic nucleotide phosphodiesterases (PDEs) to induce apoptosis and overcome glucocorticoid resistance of leukemic cells.... Stimulation of the cAMP signaling pathway has been shown to induce apoptosis and augment the effects of glucocorticoids in inducing apoptosis in leukemic... |
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SubjectTerms | Apoptosis - drug effects Apoptosis - physiology Biological and medical sciences cAMP Cyclic Nucleotide Phosphodiesterases, Type 3 - physiology Cyclic Nucleotide Phosphodiesterases, Type 4 - physiology Cyclic Nucleotide Phosphodiesterases, Type 7 - antagonists & inhibitors Cyclic Nucleotide Phosphodiesterases, Type 7 - physiology Drug Resistance, Neoplasm - drug effects Drug Resistance, Neoplasm - physiology Drug Synergism Glucocorticoids Glucocorticoids - pharmacology Hematologic and hematopoietic diseases Humans Jurkat Cells Leukemia Leukemia, T-Cell - drug therapy Leukemia, T-Cell - enzymology Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical sciences Pharmacology. Drug treatments Phosphodiesterase Phosphodiesterase 3 Inhibitors Phosphodiesterase 4 Inhibitors Phosphodiesterase Inhibitors - pharmacology Tumor Cells, Cultured |
Title | Inhibition of PDE3, PDE4 and PDE7 potentiates glucocorticoid-induced apoptosis and overcomes glucocorticoid resistance in CEM T leukemic cells |
URI | https://dx.doi.org/10.1016/j.bcp.2009.09.001 https://www.ncbi.nlm.nih.gov/pubmed/19737543 https://search.proquest.com/docview/21072908 |
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