Inhibition of MNK pathways enhances cancer cell response to chemotherapy with temozolomide and targeted radionuclide therapy
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- 作者：Michal Grzmila ; b ; michal.grzmil@psi.ch" class="auth_mail" title="E-mail the corresponding author ; Jan Seebachera ; Daniel Hessa ; Martin Beheb ; Roger Schiblib ; c ; Gerald Moncayoa ; Stephan Frankd ; Brian A. Hemmingsa
- 关键词：MNK ; MAP kinase-interacting kinase ; TMZ ; temozolomide ; GBM ; glioblastoma ; MTC ; medullary thyroid carcinoma ; ERK ; extracellular signal-regulated kinases ; eIF4E/G1 ; eukaryotic translation initiation factor 4E/G1 ; MAPK ; mitogen-activated protein kinase ; GAPDH ; glyceraldehyde 3-phosphate dehydrogenase ; HPLC ; high-performance liquid chromatography ; TMT ; tandem mass tag ; SILAC ; stable isotope labeling with amino acids ; TiO2 ; titanium dioxide ; IMAC ; immobilized metal ion affinity chromatography ; IEF ; i
- 刊名：Cellular Signalling
- 出版年：2016
- 出版时间：September 2016
- 年：2016
- 卷：28
- 期：9
- 页码：1412-1421
- 全文大小：1377 K
文摘
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Temozolomide and targeted radionuclide therapy increase MNK-dependent eIF4E phosphorylation.
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Depletion of MNK activity sensitizes glioma and MTC cells to TMZ and radiolabeled gastrin analogue.
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Phosphoproteomics analysis identified MNK inhibitor-sensitive phosphorylation sites on eIF4G1.
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MNK inhibitor-sensitive eIF4G1 phosphorylation facilitates eIF4E phosphorylation and regulates response to TMZ.
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Inhibition of MNK activity represents an attractive sensitizing strategy for chemotherapy and radiation.