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Article: Combined deficiency for MAP kinase-interacting kinase 1 and 2 (Mnk1 and Mnk2) delays tumor development

TitleCombined deficiency for MAP kinase-interacting kinase 1 and 2 (Mnk1 and Mnk2) delays tumor development
Authors
KeywordseIF4E
Mouse model
Glioma
Lymphoma
Issue Date2010
Citation
Proceedings of the National Academy of Sciences of the United States of America, 2010, v. 107, n. 32, p. 13984-13990 How to Cite?
AbstractMAP kinase-interacting kinase 1 and 2 (Mnk1 and Mnk2) are proteinserine/threonine kinases that are activated by ERK or p38 and phosphorylate eIF4E, which is involved in cap-dependent translation initiation. However, Mnk1/2 double knockout (Mnk-DKO) mice show normal cell growth and development despite an absence of eIF4E phosphorylation. Here we show that the tumorigenesis occurring in the Lck-Pten mouse model (referred to here as tPten-/- mice) can be suppressed by the loss of Mnk1/2. Phosphorylation of eIF4E was greatly enhanced in lymphomas of parental tPten-/- mice compared with lymphoid tissues of wild-type mice, but was totally absent in lymphomas of tPten-/-; Mnk-DKO mice. Notably, stable knockdown of Mnk1 in the human glioma cell line U87MG resulted in dramatically decreased tumor formation when these cells were injected into athymic nude mice. Our data demonstrate an oncogenic role for Mnk1/2 in tumor development, and highlight these molecules as potential anticancer drug targets that could be inactivated with minimal side effects.
Persistent Identifierhttp://hdl.handle.net/10722/291986
ISSN
2023 Impact Factor: 9.4
2023 SCImago Journal Rankings: 3.737
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorUeda, Takeshi-
dc.contributor.authorSasaki, Masato-
dc.contributor.authorElia, Andrew J.-
dc.contributor.authorChio, Iok In Christine-
dc.contributor.authorHamada, Koichi-
dc.contributor.authorFukunaga, Rikiro-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:55:31Z-
dc.date.available2020-11-17T14:55:31Z-
dc.date.issued2010-
dc.identifier.citationProceedings of the National Academy of Sciences of the United States of America, 2010, v. 107, n. 32, p. 13984-13990-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://hdl.handle.net/10722/291986-
dc.description.abstractMAP kinase-interacting kinase 1 and 2 (Mnk1 and Mnk2) are proteinserine/threonine kinases that are activated by ERK or p38 and phosphorylate eIF4E, which is involved in cap-dependent translation initiation. However, Mnk1/2 double knockout (Mnk-DKO) mice show normal cell growth and development despite an absence of eIF4E phosphorylation. Here we show that the tumorigenesis occurring in the Lck-Pten mouse model (referred to here as tPten-/- mice) can be suppressed by the loss of Mnk1/2. Phosphorylation of eIF4E was greatly enhanced in lymphomas of parental tPten-/- mice compared with lymphoid tissues of wild-type mice, but was totally absent in lymphomas of tPten-/-; Mnk-DKO mice. Notably, stable knockdown of Mnk1 in the human glioma cell line U87MG resulted in dramatically decreased tumor formation when these cells were injected into athymic nude mice. Our data demonstrate an oncogenic role for Mnk1/2 in tumor development, and highlight these molecules as potential anticancer drug targets that could be inactivated with minimal side effects.-
dc.languageeng-
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of America-
dc.subjecteIF4E-
dc.subjectMouse model-
dc.subjectGlioma-
dc.subjectLymphoma-
dc.titleCombined deficiency for MAP kinase-interacting kinase 1 and 2 (Mnk1 and Mnk2) delays tumor development-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1073/pnas.1008136107-
dc.identifier.pmid20679220-
dc.identifier.pmcidPMC2922567-
dc.identifier.scopuseid_2-s2.0-77956271160-
dc.identifier.volume107-
dc.identifier.issue32-
dc.identifier.spage13984-
dc.identifier.epage13990-
dc.identifier.eissn1091-6490-
dc.identifier.isiWOS:000280767700005-
dc.identifier.f10004960957-
dc.identifier.issnl0027-8424-

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