title: MNK, EIF4E and targeting translation for therapy.
abstract: Deregulation of protein translation is a common event in cancer and occurs frequently as a result of mutational activation of the AKT signaling pathway. We had previously reported the in vivo oncogenic activity of the translation initiation factor eIF4E, which acts downstream AKT and mTOR. We now identified an absolute requirement for Ser209 phosphorylation by the MNK1/2 kinases for eIF4E's oncogenic action. MNK1/2 kinases are dispensable for normal development in mammals. This potential difference between normal and cancer cells may provide a therapeutic avenue for targeting translational requirements in cancer.
authors.affiliation: Cancer Biology & Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.
authors.forename: Ricardo L A
authors.initials: RL
authors.lastname: Silva
authors.forename: Hans Guido
authors.initials: HG
authors.lastname: Wendel
mesh_terms: D000818:Animals; D039561:Eukaryotic Initiation Factor-4E / Q000378:metabolism*; D051379:Mice; D009369:Neoplasms / Q000201:enzymology* / Q000628:therapy*; D010766:Phosphorylation; D014176:Protein Biosynthesis; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*
chemical_list: D039561:Eukaryotic Initiation Factor-4E; C106281:Mknk1 protein, mouse; C106282:Mknk2 protein, mouse; D017346:Protein Serine-Threonine Kinases