The direct Myc target Pim3 cooperates with other Pim kinases in supporting viability of Myc-induced B-cell lymphomas
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;
Jonas Nilsson, e-mail:
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.
Linus Plym Forshell
Tacha Zi Plym Forshell
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