PIM kinases as potential therapeutic targets in a subset of peripheral T cell lymphoma cases

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dc.contributor.author	Martín-Sánchez, Esperanza
dc.contributor.author	Real, Francisco X.
dc.contributor.author	Piris, Miguel A.
dc.date	2014
dc.identifier.citation	Martín-Sánchez E, Odqvist L, Rodríguez-Pinilla SM, Sánchez-Beato M, Roncador G, Domínguez-González B et al. PIM kinases as potential therapeutic targets in a subset of peripheral T cell lymphoma cases. PLoS One. 2014; 9(11): e112148. DOI 10.1371/journal.pone.0112148
dc.identifier.citation	1932-6203
dc.identifier.citation	http://dx.doi.org/10.1371/journal.pone.0112148
dc.identifier.uri	http://hdl.handle.net/10230/23705
dc.format	application/pdf
dc.language.iso	eng
dc.publisher	Public Library of Science (PLoS)
dc.relation	PLoS One. 2014; 9(11): e112148
dc.relation	info:eu-repo/grantAgreement/ES/3PN/SAF2008-0387
dc.rights	© 2014 Martín-Sánchez et al. 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
dc.rights	info:eu-repo/semantics/openAccess
dc.subject	Transducció de senyal cel·lular
dc.subject	Cèl·lules -- Interacció
dc.title	PIM kinases as potential therapeutic targets in a subset of peripheral T cell lymphoma cases
dc.type	info:eu-repo/semantics/article
dc.type	info:eu-repo/semantics/publishedVersion
dc.description.abstract	Currently, there is no efficient therapy for patients with peripheral T cell lymphoma (PTCL). The Proviral Integration site of Moloney murine leukemia virus (PIM) kinases are important mediators of cell survival. We aimed to determine the therapeutic value of PIM kinases because they are overexpressed in PTCL patients, T cell lines and primary tumoral T cells. PIM kinases were inhibited genetically (using small interfering and short hairpin RNAs) and pharmacologically (mainly with the pan-PIM inhibitor (PIMi) ETP-39010) in a panel of 8 PTCL cell lines. Effects on cell viability, apoptosis, cell cycle, key proteins and gene expression were evaluated. Individual inhibition of each of the PIM genes did not affect PTCL cell survival, partially because of a compensatory mechanism among the three PIM genes. In contrast, pharmacological inhibition of all PIM kinases strongly induced apoptosis in all PTCL cell lines, without cell cycle arrest, in part through the induction of DNA damage. Therefore, pan-PIMi synergized with Cisplatin. Importantly, pharmacological inhibition of PIM reduced primary tumoral T cell viability without affecting normal T cells ex vivo. Since anaplastic large cell lymphoma (ALK+ ALCL) cell lines were the most sensitive to the pan-PIMi, we tested the simultaneous inhibition of ALK and PIM kinases and found a strong synergistic effect in ALK+ ALCL cell lines. Our findings suggest that PIM kinase inhibition could be of therapeutic value in a subset of PTCL, especially when combined with ALK inhibitors, and might be clinically beneficial in ALK+ ALCL.
dc.description.abstract	This work was supported by grants from the Asociación Española Contra el Cáncer, Fondo de Investigaciones Sanitarias (PI051623, PI052800 and FIS11/1759), RTICC (RD06/0020/0107) and Ministerio de Ciencia e Innovación (SAF2008-0387-1). EMS was supported by a grant from the Department of Education, Universities and Research of the Basque Government (BFI08.207). MSB was supported by a Contract Miguel Servet from Fondo de Investigaciones Sanitarias (CP11/00018).

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