ArticleNature communications2018
Fatty Acid Synthase induced S6Kinase facilitates USP11-eIF4B complex formation for sustained oncogenic translation in DLBCL.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
57 citing papers in PubMed, 101 citations in OpenAlex.
- PTBP1-Mediated Alternative Splicing of DNAJB6 Promotes Everolimus Resistance in Clear Cell Renal Cell Carcinoma via EIF4B/PKIB/AKT/mTOR Positive Feedback Loop.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Lipid Metabolism Reprogramming in Diffuse Large B-Cell Lymphoma (DLBCL): Mechanisms and Treatment Strategies.Cancers · 2026Review
- Identification of a fatty acid metabolism-related gene signature for prognostic prediction and immune microenvironment characterization in diffuse large B-cell lymphoma.Frontiers in oncology · 2026Article
- Fatty acid metabolic signature reveals FASN as an immunosuppressive factor in DLBCL tumor microenvironment.Medical oncology (Northwood, London, England) · 2025Article
- Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025Review
- Tumor Microenvironment, Inflammation, and Inflammatory Prognostic Indices in Diffuse Large B-Cell Lymphomas: A Narrative Review.International journal of molecular sciences · 2025Review
- Article
- Fatty Acid Metabolism Provides an Essential Survival Signal in OxPhos and BCR DLBCL Cells.Biomedicines · 2025Article
- PIWIL2/PDK1 Axis Promotes the Progression of Cervical Epithelial Lesions via Metabolic Reprogramming to Maintain Tumor-Initiating Cell Stemness.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Eukaryotic initiation factor 4B is a multi-functional RNA binding protein that regulates histone mRNAs.Nucleic acids research · 2024Article
- Targeting YTHDF2 inhibits tumorigenesis of diffuse large B-cell lymphoma through ACER2-mediated ceramide catabolism.Journal of advanced research · 2024Article
- USP11 promotes prostate cancer progression by up-regulating AR and c-Myc activity.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Fatty Acid Synthase Promotes Hepatocellular Carcinoma Growth via S-Phase Kinase-Associated Protein 2/p27Medicina (Kaunas, Lithuania) · 2024Article
- Article
- RNA helicase EIF4A1-mediated translation is essential for the GC response.Life science alliance · 2024Article
- A novel lipid metabolism-based risk model associated with immunosuppressive mechanisms in diffuse large B-cell lymphoma.Lipids in health and disease · 2024Article
- USP11 promotes glycolysis by regulating HIF-1α stability in hepatocellular carcinoma.Journal of cellular and molecular medicine · 2024Article
- Role of EGFR and FASN in breast cancer progression.Journal of cell communication and signaling · 2023Review
- Deubiquitylating Enzymes in Cancer and Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Deubiquitinases in cancer.Nature reviews. Cancer · 2023Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Altered lipid metabolism and aberrant protein translation are strongly associated with cancerous outgrowth; however, the inter-regulation of these key processes is still underexplored in diffuse large B-cell lymphoma (DLBCL). Although fatty acid synthase (FASN) activity is reported to positively correlate with PI3K-Akt-mTOR pathway that can modulate protein synthesis, the precise impact of FASN inhibition on this process is still unknown. Herein, we demonstrate that attenuating FASN expression or its activity significantly reduces eIF4B (eukaryotic initiation factor 4B) levels and consequently overall protein translation. Through biochemical studies, we identified eIF4B as a bonafide substrate of USP11, which stabilizes and enhances eIF4B activity. Employing both pharmacological and genetic approaches, we establish that FASN-induced PI3K-S6Kinase signaling phosphorylates USP11 enhancing its interaction with eIF4B and thereby promoting oncogenic translation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.