ArticleHepatology (Baltimore, Md.)2016
PI3K/AKT/mTOR-dependent stabilization of oncogenic far-upstream element binding proteins in hepatocellular carcinoma cells.
Article in Hepatology (Baltimore, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 83 citations in OpenAlex.
- FUBL-3/FUBP1 mediates mitochondrial stress-induced chromatin remodeling and longevity.Science advances · 2026Article
- Targeting SRC to mediate solasonine's anti-cancer activity in hepatocellular carcinoma and its potential for multi-cancer therapy.Frontiers in oncology · 2026Article
- Integrated mRNA and miRNA Analysis Reveals Layer-Specific Mechanisms of Antler Yield Variation in Sika Deer.Animals : an open access journal from MDPI · 2025Article
- The role of fructose-1,6-bisphosphatase 1 on regulating the cancer progression and drug resistance.Discover oncology · 2025Review
- Hepatocellular carcinoma: signaling pathways and therapeutic advances.Signal transduction and targeted therapy · 2025Review
- PRMT5-mediated FUBP1 methylation accelerates prostate cancer progression.The Journal of clinical investigation · 2024Article
- Lecithin-cholesterol acyltransferase is a potential tumor suppressor and predictive marker for hepatocellular carcinoma metastasis.World journal of gastrointestinal oncology · 2024Article
- Targeting EGFR/PI3K/AKT/mTOR Signaling in Hepatocellular Carcinoma.Pharmaceutics · 2023Review
- Application of multi-modality MRI-based radiomics in the pre-treatment prediction of RPS6K expression in hepatocellular carcinoma.Molecular biomedicine · 2023Article
- Regulatory Role of Ribonucleotide Reductase Subunit M2 in Hepatocyte Growth and Pathogenesis of Hepatitis C Virus.International journal of molecular sciences · 2023Review
- Inhibition of eIF6 Activity Reduces Hepatocellular Carcinoma Growth: An In Vivo and In Vitro Study.International journal of molecular sciences · 2022Article
- mTOR regulates aerobic glycolysis through NEAT1 and nuclear paraspeckle-mediated mechanism in hepatocellular carcinoma.Theranostics · 2022Article
- G-Protein-Coupled Receptor Kinase-Interacting Protein 1 (GIT1) Promotes Head and Neck Squamous Cell Carcinoma Metastases via Activating the PI3K/AKT/mTOR Signal Pathway.Computational and mathematical methods in medicine · 2022Article
- Dairy consumption and hepatocellular carcinoma risk.Annals of translational medicine · 2021Review
- Differentially Expressed Long Noncoding RNAs Involved in FUBP1 Promoting Hepatocellular Carcinoma Cells Proliferation.BioMed research international · 2021Article
- Combined Scutellarin and CFrontiers in oncology · 2021Article
- MicroRNA-92b augments sorafenib resistance in hepatocellular carcinoma via targeting PTEN to activate PI3K/AKT/mTOR signaling.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021Article
- TNPO1-Mediated Nuclear Import of FUBP1 Contributes to Tumor Immune Evasion by Increasing NRP1 Expression in Cervical Cancer.Journal of immunology research · 2021Article
- Overexpression of GINS4 Is Associated With Tumor Progression and Poor Survival in Hepatocellular Carcinoma.Frontiers in oncology · 2021Article
- Role of long noncoding RNA-mediated competing endogenous RNA regulatory network in hepatocellular carcinoma.World journal of gastroenterology · 2020Review
Corrections and comments
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Authors and funding
18 authors at 9 institutions in 3 countries.
Funding
Abstract
unlabelledTranscription factors of the far-upstream element-binding protein (FBP) family represent cellular pathway hubs, and their overexpression in liver cancer (hepatocellular carcinoma [HCC]) stimulates tumor cell proliferation and correlates with poor prognosis. Here we determine the mode of oncogenic FBP overexpression in HCC cells. Using perturbation approaches (kinase inhibitors, small interfering RNAs) and a novel system for rapalog-dependent activation of AKT isoforms, we demonstrate that activity of the phosphatidylinositol-4,5-biphosphate 3-kinase/AKT pathway is involved in the enrichment of nuclear FBP1 and FBP2 in liver cancer cells. In human HCC tissues, phospho-AKT significantly correlates with nuclear FBP1/2 accumulation and expression of the proliferation marker KI67. Mechanistic target of rapamycin (mTOR) inhibition or blockade of its downstream effector eukaryotic translation initiation factor 4E activity equally reduced FBP1/2 concentrations. The mTORC1 inhibitor rapamycin diminishes FBP enrichment in liver tumors after hydrodynamic gene delivery of AKT plasmids. In addition, the multikinase inhibitor sorafenib significantly reduces FBP levels in HCC cells and in multidrug resistance 2-deficient mice that develop HCC due to severe inflammation. Both FBP1/2 messenger RNAs are highly stable, with FBP2 being more stable than FBP1. Importantly, inhibition of phosphatidylinositol-4,5-biphosphate 3-kinase/AKT/mTOR signaling significantly diminishes FBP1/2 protein stability in a caspase-3/-7-dependent manner.
conclusionThese data provide insight into a transcription-independent mechanism of FBP protein enrichment in liver cancer; further studies will have to show whether this previously unknown interaction between phosphatidylinositol-4,5-biphosphate 3-kinase/AKT/mTOR pathway activity and caspase-mediated FBP stabilization allows the establishment of interventional strategies in FBP-positive HCCs.
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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.