The tumor suppressor PP2A is functionally inactivated in blast crisis CML through the inhibitory activity of the BCR/ABL-regulated SET protein
The oncogenic BCR/ABL kinase activity induces and maintains chronic myelogenous leukemia (CML). We show here that, in BCR/ABL-transformed cells and CML blast crisis (CML-BC) progenitors, the phosphatase activity of the tumor suppressor PP2A is inhibited by the BCR/ABL-induced expression of the PP2A...
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| Published in | Cancer cell Vol. 8; no. 5; pp. 355 - 368 |
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| Main Authors | , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.11.2005
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| Subjects | |
| Online Access | Get full text |
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| Abstract | The oncogenic BCR/ABL kinase activity induces and maintains chronic myelogenous leukemia (CML). We show here that, in BCR/ABL-transformed cells and CML blast crisis (CML-BC) progenitors, the phosphatase activity of the tumor suppressor PP2A is inhibited by the BCR/ABL-induced expression of the PP2A inhibitor SET. In imatinib-sensitive and -resistant (T315I included) BCR/ABL
+ cell lines and CML-BC progenitors, molecular and/or pharmacological activation of PP2A promotes dephosphorylation of key regulators of cell proliferation and survival, suppresses BCR/ABL activity, and induces BCR/ABL degradation. Furthermore, PP2A activation results in growth suppression, enhanced apoptosis, restored differentiation, impaired clonogenic potential, and decreased in vivo leukemogenesis of imatinib-sensitive and -resistant BCR/ABL
+ cells. Thus, functional inactivation of PP2A is essential for BCR/ABL leukemogenesis and, perhaps, required for blastic transformation. |
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| AbstractList | The oncogenic BCR/ABL kinase activity induces and maintains chronic myelogenous leukemia (CML). We show here that, in BCR/ABL-transformed cells and CML blast crisis (CML-BC) progenitors, the phosphatase activity of the tumor suppressor PP2A is inhibited by the BCR/ABL-induced expression of the PP2A inhibitor SET. In imatinib-sensitive and -resistant (T315I included) BCR/ABL
+ cell lines and CML-BC progenitors, molecular and/or pharmacological activation of PP2A promotes dephosphorylation of key regulators of cell proliferation and survival, suppresses BCR/ABL activity, and induces BCR/ABL degradation. Furthermore, PP2A activation results in growth suppression, enhanced apoptosis, restored differentiation, impaired clonogenic potential, and decreased in vivo leukemogenesis of imatinib-sensitive and -resistant BCR/ABL
+ cells. Thus, functional inactivation of PP2A is essential for BCR/ABL leukemogenesis and, perhaps, required for blastic transformation. The oncogenic BCR/ABL kinase activity induces and maintains chronic myelogenous leukemia (CML). We show here that, in BCR/ABL-transformed cells and CML blast crisis (CML-BC) progenitors, the phosphatase activity of the tumor suppressor PP2A is inhibited by the BCR/ABL-induced expression of the PP2A inhibitor SET. In imatinib-sensitive and -resistant (T315I included) BCR/ABL+ cell lines and CML-BC progenitors, molecular and/or pharmacological activation of PP2A promotes dephosphorylation of key regulators of cell proliferation and survival, suppresses BCR/ABL activity, and induces BCR/ABL degradation. Furthermore, PP2A activation results in growth suppression, enhanced apoptosis, restored differentiation, impaired clonogenic potential, and decreased in vivo leukemogenesis of imatinib-sensitive and -resistant BCR/ABL+ cells. Thus, functional inactivation of PP2A is essential for BCR/ABL leukemogenesis and, perhaps, required for blastic transformation. |
| Author | Santhanam, Ramasamy Marcucci, Guido Blaser, Bradley W. Bruner-Klisovic, Rebecca Mao, Hsiaoyin Galietta, Annamaria Perrotti, Danilo Trotta, Rossana Neviani, Paolo Liu, Shujun Uttam, Ashwin Caligiuri, Michael A. Valtieri, Mauro Notari, Mario Chang, Ji Suk Roy, Denis C. Bloomfield, Clara D. |
| Author_xml | – sequence: 1 givenname: Paolo surname: Neviani fullname: Neviani, Paolo organization: Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, Ohio 43210 – sequence: 2 givenname: Ramasamy surname: Santhanam fullname: Santhanam, Ramasamy organization: Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, Ohio 43210 – sequence: 3 givenname: Rossana surname: Trotta fullname: Trotta, Rossana organization: Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, Ohio 43210 – sequence: 4 givenname: Mario surname: Notari fullname: Notari, Mario organization: Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, Ohio 43210 – sequence: 5 givenname: Bradley W. surname: Blaser fullname: Blaser, Bradley W. organization: Division of Hematology/Oncology, Department of Internal Medicine, The Ohio State University, Columbus, Ohio 43210 – sequence: 6 givenname: Shujun surname: Liu fullname: Liu, Shujun organization: Division of Hematology/Oncology, Department of Internal Medicine, The Ohio State University, Columbus, Ohio 43210 – sequence: 7 givenname: Hsiaoyin surname: Mao fullname: Mao, Hsiaoyin organization: Division of Hematology/Oncology, Department of Internal Medicine, The Ohio State University, Columbus, Ohio 43210 – sequence: 8 givenname: Ji Suk surname: Chang fullname: Chang, Ji Suk organization: Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, Ohio 43210 – sequence: 9 givenname: Annamaria surname: Galietta fullname: Galietta, Annamaria organization: Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, Ohio 43210 – sequence: 10 givenname: Ashwin surname: Uttam fullname: Uttam, Ashwin organization: Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, Ohio 43210 – sequence: 11 givenname: Denis C. surname: Roy fullname: Roy, Denis C. organization: Division of Hematology-Immunology, Maisonneuve-Rosemont Hospital Research Center, Department of Medicine, Université de Montreal, Montreal, Quebec, Canada H1T 2M4 – sequence: 12 givenname: Mauro surname: Valtieri fullname: Valtieri, Mauro organization: Department of Hematology-Oncology, Istituto Superiore di Sanitá, Rome, Italy 00161 – sequence: 13 givenname: Rebecca surname: Bruner-Klisovic fullname: Bruner-Klisovic, Rebecca organization: Division of Hematology/Oncology, Department of Internal Medicine, The Ohio State University, Columbus, Ohio 43210 – sequence: 14 givenname: Michael A. surname: Caligiuri fullname: Caligiuri, Michael A. organization: Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, Ohio 43210 – sequence: 15 givenname: Clara D. surname: Bloomfield fullname: Bloomfield, Clara D. organization: Division of Hematology/Oncology, Department of Internal Medicine, The Ohio State University, Columbus, Ohio 43210 – sequence: 16 givenname: Guido surname: Marcucci fullname: Marcucci, Guido organization: Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, Ohio 43210 – sequence: 17 givenname: Danilo surname: Perrotti fullname: Perrotti, Danilo email: danilo.perrotti@osumc.edu organization: Human Cancer Genetics Program, Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University, Columbus, Ohio 43210 |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16286244$$D View this record in MEDLINE/PubMed |
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| Snippet | The oncogenic BCR/ABL kinase activity induces and maintains chronic myelogenous leukemia (CML). We show here that, in BCR/ABL-transformed cells and CML blast... |
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| SubjectTerms | Animals Antineoplastic Agents - pharmacology Benzamides Blast Crisis - metabolism Cell Line, Transformed Chromosomal Proteins, Non-Histone - physiology Colforsin - pharmacology Enzyme Inhibitors - metabolism Fusion Proteins, bcr-abl - physiology Histone Chaperones Humans Imatinib Mesylate In Vitro Techniques K562 Cells Leukemia - prevention & control Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology Mice Mice, SCID Neoplasm Transplantation Phosphoprotein Phosphatases - antagonists & inhibitors Phosphoprotein Phosphatases - metabolism Phosphoprotein Phosphatases - physiology Piperazines - pharmacology Protein Phosphatase 2 Pyrimidines - pharmacology Transcription Factors - physiology Tumor Cells, Cultured Tumor Suppressor Proteins - antagonists & inhibitors Tumor Suppressor Proteins - physiology |
| Title | The tumor suppressor PP2A is functionally inactivated in blast crisis CML through the inhibitory activity of the BCR/ABL-regulated SET protein |
| URI | https://dx.doi.org/10.1016/j.ccr.2005.10.015 https://www.ncbi.nlm.nih.gov/pubmed/16286244 https://search.proquest.com/docview/19730329 https://search.proquest.com/docview/68803090 |
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