The direct Myc target Pim3 cooperates with other Pim kinases in supporting viability of Myc-induced B-cell lymphomas.
| Title: | The direct Myc target Pim3 cooperates with other Pim kinases in supporting viability of Myc-induced B-cell lymphomas. |
|---|---|
| Authors: | Forshell LP; Department of Molecular Biology, Umeå University, Umeå, Sweden.; Li Y; Forshell TZ; Rudelius M; Nilsson L; Keller U; Nilsson J |
| Source: | Oncotarget [Oncotarget] 2011 Jun; Vol. 2 (6), pp. 448-60. |
| Publication Type: | Journal Article; Research Support, Non-U.S. Gov't |
| Language: | English |
| Journal Info: | Publisher: Impact Journals Country of Publication: United States NLM ID: 101532965 Publication Model: Print Cited Medium: Internet ISSN: 1949-2553 (Electronic) Linking ISSN: 19492553 NLM ISO Abbreviation: Oncotarget Subsets: MEDLINE |
| Imprint Name(s): | Original Publication: Albany, N.Y. : Impact Journals |
| MeSH Terms: | Cell Transformation, Neoplastic/*genetics ; Lymphoma, B-Cell/*genetics ; Lymphoma, B-Cell/*pathology ; Protein Serine-Threonine Kinases/*physiology ; Proto-Oncogene Proteins/*physiology ; Proto-Oncogene Proteins c-myc/*physiology ; Proto-Oncogene Proteins c-pim-1/*physiology; Caspase 3/metabolism ; Cell Survival/drug effects ; Cell Survival/genetics ; Cell Transformation, Neoplastic/drug effects ; Cell Transformation, Neoplastic/pathology ; Gene Expression Regulation, Neoplastic/drug effects ; Protein Kinase Inhibitors/pharmacology ; Protein Serine-Threonine Kinases/antagonists & inhibitors ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/antagonists & inhibitors ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Proto-Oncogene Proteins c-pim-1/antagonists & inhibitors ; Proto-Oncogene Proteins c-pim-1/genetics ; Proto-Oncogene Proteins c-pim-1/metabolism ; Animals ; Cell Line, Tumor ; Humans ; Mice ; Mice, Transgenic ; NIH 3T3 Cells |
| Abstract: | The Pim kinases are weak oncogenes. However, when co-expressed with a strong oncogene, such as c-Myc, Pim kinases potentiate the oncogenic effect resulting in an acceleration of tumorigenesis. In this study we show that the least studied Pim kinase, Pim-3, is encoded by a gene directly regulated by c-Myc via binding to one of the conserved E-boxes within the Pim3 gene. Accordingly, lymphomas arising in Myc-transgenic mice and Burkitt lymphoma cell lines exhibit elevated levels of Pim-3. Interestingly, inhibition of Pim kinases by a novel pan-Pim kinase inhibitor, Pimi, in Myc-induced lymphoma results in cell death that appears independent of caspases. The data indicate that Pim kinase inhibition could be a viable treatment strategy in certain human lymphomas that rely on Pim-3 kinase expression. |
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| Substance Nomenclature: | 0 (Protein Kinase Inhibitors); 0 (Proto-Oncogene Proteins); 0 (Proto-Oncogene Proteins c-myc); EC 2.7.11.1 (PIM3 protein, human); EC 2.7.11.1 (Protein Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-pim-1); EC 2.7.11.1 (proto-oncogene proteins pim); EC 3.4.22.- (Caspase 3) |
| Entry Date(s): | Date Created: 20110608 Date Completed: 20111108 Latest Revision: 20211203 |
| Update Code: | 20260130 |
| PubMed Central ID: | PMC3248204 |
| DOI: | 10.18632/oncotarget.283 |
| PMID: | 21646687 |
| Database: | MEDLINE |
Journal Article; Research Support, Non-U.S. Gov't