Oncotarget

Research Papers:

The direct Myc target Pim3 cooperates with other Pim kinases in supporting viability of Myc-induced B-cell lymphomas

Linus Plym Forshell, Yongmei Li, Tacha Zi Plym Forshell, Martina Rudelius, Lisa Nilsson, Ulrich Keller and Jonas Nilsson _

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Oncotarget. 2011; 2:448-460. https://doi.org/10.18632/oncotarget.283

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Abstract

Linus Plym Forshell1, Yongmei Li1,2,*, Tacha Zi Plym Forshell1, *, Martina Rudelius3, Lisa Nilsson1, Ulrich Keller4 and Jonas Nilsson1

1 Department of Molecular Biology, Umeå University, Umeå, Sweden

2Department of Medical Microbiology, Tianjin Medical University, Tianjin, People's Republic of China

3Department of Pathology, Technical University of Munich, Munich, Germany

4Department of Medicine, Technical University of Munich, Munich, Germany

*Denotes equal contribution

Keywords: cancer, lymphoma, oncogenes, c-Myc, Pim-3

Received: June 1, 2011; Accepted: June 2, 2011; Published: June 5, 2011;

Correspondence:

Jonas Nilsson, e-mail:

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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