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

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...

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Main Authors:	Forshell, Linus Plym, Li, Yongmei, Forshell, Tacha Zi Plym, Rudelius, Martina, Nilsson, Lisa, Keller, Ulrich, Nilsson, Jonas
Format:	Online
Language:	English
Published:	Impact Journals LLC 2011
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248204/

id	pubmed-3248204
recordtype	oai_dc
spelling	pubmed-32482042012-01-18 The direct Myc target Pim3 cooperates with other Pim kinases in supporting viability of Myc-induced B-cell lymphomas Forshell, Linus Plym Li, Yongmei Forshell, Tacha Zi Plym Rudelius, Martina Nilsson, Lisa Keller, Ulrich Nilsson, Jonas Research Papers 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. Impact Journals LLC 2011-06-05 /pmc/articles/PMC3248204/ /pubmed/21646687 Text en Copyright: © 2011 Forshell et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Forshell, Linus Plym Li, Yongmei Forshell, Tacha Zi Plym Rudelius, Martina Nilsson, Lisa Keller, Ulrich Nilsson, Jonas
spellingShingle	Forshell, Linus Plym Li, Yongmei Forshell, Tacha Zi Plym Rudelius, Martina Nilsson, Lisa Keller, Ulrich Nilsson, Jonas The direct Myc target Pim3 cooperates with other Pim kinases in supporting viability of Myc-induced B-cell lymphomas
author_facet	Forshell, Linus Plym Li, Yongmei Forshell, Tacha Zi Plym Rudelius, Martina Nilsson, Lisa Keller, Ulrich Nilsson, Jonas
author_sort	Forshell, Linus Plym
title	The direct Myc target Pim3 cooperates with other Pim kinases in supporting viability of Myc-induced B-cell lymphomas
title_short	The direct Myc target Pim3 cooperates with other Pim kinases in supporting viability of Myc-induced B-cell lymphomas
title_full	The direct Myc target Pim3 cooperates with other Pim kinases in supporting viability of Myc-induced B-cell lymphomas
title_fullStr	The direct Myc target Pim3 cooperates with other Pim kinases in supporting viability of Myc-induced B-cell lymphomas
title_full_unstemmed	The direct Myc target Pim3 cooperates with other Pim kinases in supporting viability of Myc-induced B-cell lymphomas
title_sort	direct myc target pim3 cooperates with other pim kinases in supporting viability of myc-induced b-cell lymphomas
description	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.
publisher	Impact Journals LLC
publishDate	2011
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3248204/
_version_	1611497304809799680

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

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