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Mitotic MELK-eIF4B signaling controls protein synthesis and tumor cell survival
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Mitotic MELK-eIF4B signaling controls protein synthesis and tumor cell survival
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Journal Article
Mitotic MELK-eIF4B signaling controls protein synthesis and tumor cell survival
2016
Overview
The protein kinase maternal and embryonic leucine zipper kinase (MELK) is critical for mitotic progression of cancer cells; however, its mechanisms of action remain largely unknown. By combined approaches of immunoprecipitation/mass spectrometry and peptide library profiling, we identified the eukaryotic translation initiation factor 4B (eIF4B) as a MELK-interacting protein during mitosis and a bona fide substrate of MELK. MELK phosphorylates eIF4B at Ser406, a modification found to be most robust in the mitotic phase of the cell cycle. We further show that the MELK–eIF4B signaling axis regulates protein synthesis during mitosis. Specifically, synthesis of myeloid cell leukemia 1 (MCL1), an antiapoptotic protein known to play a role in cancer cell survival during cell division, depends on the function of MELK-eIF4B. Inactivation of MELK or eIF4B results in reduced protein synthesis of MCL1, which, in turn, induces apoptotic cell death of cancer cells. Our study thus defines a MELK–eIF4B signaling axis that regulates protein synthesis during mitosis, and consequently influences cancer cell survival.
Publisher
National Academy of Sciences
Subject
/ Animals
/ Eukaryotic Initiation Factors - antagonists & inhibitors
/ Eukaryotic Initiation Factors - genetics
/ Eukaryotic Initiation Factors - metabolism
/ Humans
/ Leukemia
/ Mitosis
/ Myeloid Cell Leukemia Sequence 1 Protein - genetics
/ Myeloid Cell Leukemia Sequence 1 Protein - metabolism
/ Protein-Serine-Threonine Kinases - antagonists & inhibitors
/ Protein-Serine-Threonine Kinases - genetics
/ Protein-Serine-Threonine Kinases - metabolism
/ RNA, Small Interfering - genetics
/ RNA, Small Interfering - metabolism
/ Tumors
