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MNK, EIF4E and targeting translation for therapy

Ricardo L.A. Silva and Hans-Guido Wendel

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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

Ricardo L.A. Silva

Memorial Sloan-Kettering Cancer Center; New York, NY

Hans-Guido Wendel

Memorial Sloan-Kettering Cancer Center; New York, NY

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Subscribe to this journal for $129/year