ArticleCell systems2021
Deep computational analysis details dysregulation of eukaryotic translation initiation complex eIF4F in human cancers.
Article in Cell systems, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Targeting eIF4A-dependent translation in genetically complex sarcoma.JCI insight · 2026Article
- Article
- The EIF4EBP1 gene encoding 4EBP1 is transcriptionally upregulated by MYC and linked to shorter survival in medulloblastoma.Cell death discovery · 2025Article
- SRSF6 modulates histone-chaperone HIRA splicing to orchestrate AR and E2F activity in prostate cancer.Science advances · 2024Article
- mTORC1 regulates cell survival under glucose starvation through 4EBP1/2-mediated translational reprogramming of fatty acid metabolism.Nature communications · 2024Article
- Computational inference of eIF4F complex function and structure in human cancers.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Protocol to analyze dysregulation of the eIF4F complex in human cancers using R software and large public datasets.STAR protocols · 2022Article
- EIF4G1 Is a Potential Prognostic Biomarker of Breast Cancer.Biomolecules · 2022Article
- Identification of N7-methylguanosine related signature for prognosis and immunotherapy efficacy prediction in lung adenocarcinoma.Frontiers in medicine · 2022Article
- Integrative pan-cancer analysis and clinical characterization of the N7-methylguanosine (m7G) RNA modification regulators in human cancers.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
eIF4F plays diverse roles in human cancers, which complicate the development of an overarching understanding of its functional and regulatory impacts across tumor types. Typically, eIF4F drives initiation from the mRNA 5' end (cap) and is composed of eIF4G1, eIF4A1, and cap-binding eIF4E. Cap-independent initiation is possible without eIF4E, from internal ribosomal entry sites (IRESs). By analyzing large public datasets, we found that cancers selectively overexpress EIF4G1 more than EIF4E. That expression imbalance supports EIF4G1 as a prognostic indicator in patients with cancer. It also attenuates "housekeeping" pathways that are usually regulated in a tissue-specific manner via cap-dependent initiation in healthy tissues and reinforce regulation of cancer-preferred pathways in cap-independent contexts. Cap-independent initiation is mechanistically attributable to eIF4G1 hyperphosphorylation that promotes binding to eIF4A1 and reduced eIF4E availability. Collectively, these findings reveal a novel model of dysregulated eIF4F function and highlight the clinical relevance of cap-(in)dependent initiation in cancer.
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