ArticleCell death & disease2026
EIF4B Ser93 phosphorylation by ERK2 promotes epithelial-mesenchymal transition to drive colorectal cancer metastasis.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Differential analysis of urinary stable downregulated proteins in male patients after colorectal cancer surgery.Frontiers in oncology · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
Colorectal cancer (CRC) is the third most common malignant tumor and the second leading cause of cancer-related mortality globally. Epithelial to mesenchymal transition (EMT) contributes to CRC metastasis and poor prognosis. Aberrant protein phosphorylation is implicated in CRC progression, warranting further investigation into its molecular mechanisms. Herein, we have identified significant alterations in protein phosphorylation associated with CRC through tandem mass tag (TMT) label-based phosphoproteomic analysis. The functions and enriched signaling pathways of these proteins were predominantly linked to the EMT process. Notably, the phosphorylation of eIF4B at Ser93 exhibited the most pronounced increase in CRC, a finding that was further validated in CRC tissues and cell lines by a newly generated antibody targeting eIF4B Ser93 phosphorylation. Phosphorylation of eIF4B Ser93 promoted CRC progression and metastasis both in vitro and in vivo. Mechanistically, eIF4B Ser93 phosphorylation decreased ubiquitination-mediated eIF4B degradation and enhanced its translation activity, through which it facilitated the translation of mesenchymal markers. Additionally, ERK2 directly phosphorylated eIF4B at Ser93, while inhibiting this phosphorylation is essential for the anti-cancer efficacy of the ERK2 inhibitor, Vx-11e. Together, the phosphorylation of eIF4B Ser93 driven by ERK2 promotes CRC growth and metastasis through the activation of EMT. Our findings indicate a novel therapeutic target and provide promising strategies for clinical intervention in human CRC.
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