ArticleNature communications2018
The tumor suppressor menin prevents effector CD8 T-cell dysfunction by targeting mTORC1-dependent metabolic activation.
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 52 papers.
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Who cites it
52 citing papers in PubMed, 82 citations in OpenAlex.
- Article
- Overview of glutamine metabolism in stromal components of the tumor microenvironment and potential anti-tumor therapies.Genes & diseases · 2026Review
- Mitochondria in T‑cell tumor immunity and tumor therapies targeting mitochondria (Review).Oncology reports · 2026Review
- Single-cell profiling reveals immunometabolic remodeling with T-cell dysfunction in HIV-1 infected people.Infectious diseases & immunity · 2026Article
- Nanomaterials Reshaping Tumor Metabolism: A New Frontier to Overcome T Cell Exhaustion.International journal of nanomedicine · 2026Review
- Glutamine Metabolism: Role in Cancer Cell Proliferation and Survival.Cancer treatment and research · 2026Review
- The role of hormonal and nutritional biomarkers in predicting immune checkpoint inhibitor efficacy: current limitations and future prospects.Frontiers in immunology · 2026Review
- Menin-driven mTOR signaling sustains taxane resistance in CRPC and reveals a targetable vulnerability for combination therapy.Cell communication and signaling : CCS · 2025Article
- Epigenetic drugs in cancer therapy: mechanisms, immune modulation, and therapeutic applications.Molecular biomedicine · 2025Review
- The Pathogenic Role of T Cell Metabolism and its Effect on Immune Senescence in Autoimmune Diseases and Infection.Clinical reviews in allergy & immunology · 2025Review
- Envirotune-CAR-T: a hypoxia-responsive and glutamine-enhanced CAR-T cell therapy for overcoming tumor microenvironment-mediated suppression.Journal for immunotherapy of cancer · 2025Article
- Integrative machine learning reveals the biological function and prognostic significance of α-ketoglutarate in gastric cancer.Oncology letters · 2025Article
- Targeting metabolic dysfunction of CD8 T cells and natural killer cells in cancer.Nature reviews. Drug discovery · 2025Review
- Glutamine and cancer: metabolism, immune microenvironment, and therapeutic targets.Cell communication and signaling : CCS · 2025Review
- Mannose metabolism reshapes T cell differentiation to enhance anti-tumor immunity.Cancer cell · 2025Article
- TSC1 deficiency drives immune evasion in colorectal cancer via mTORC1-mediated dysregulation of PD-L1 sialylation.Frontiers in immunology · 2025Article
- CCL26-CX3CR1 Axis Mediates a Feedback Loop between Cancer Cell and PMN-MDSCs to Promote CD8Research (Washington, D.C.) · 2025Article
- Sodium chloride in the tumor microenvironment enhances T cell metabolic fitness and cytotoxicity.Nature immunology · 2024Article
- Cellular senescence by loss of Men1 in osteoblasts is critical for age-related osteoporosis.Aging cell · 2024Article
- MEN1 deficiency stabilizes PD-L1 and promotes tumor immune evasion of lung cancer.Cancer science · 2024Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While menin plays an important role in preventing T-cell dysfunction, such as senescence and exhaustion, the regulatory mechanisms remain unclear. We found that menin prevents the induction of dysfunction in activated CD8 T cells by restricting the cellular metabolism. mTOR complex 1 (mTORC1) signaling, glycolysis, and glutaminolysis are augmented by menin deficiency. Rapamycin treatment prevents CD8 T-cell dysfunction in menin-deficient CD8 T cells. Limited glutamine availability also prevents CD8 T-cell dysfunction induced by menin deficiency, and its inhibitory effect is antagonized by α-ketoglutarate (α-KG), an intermediate metabolite of glutaminolysis. α-KG-dependent histone H3K27 demethylation seems to be involved in the dysfunction in menin-deficient CD8 T cells. We also found that α-KG activates mTORC1-dependent central carbon metabolism. These findings suggest that menin maintains the T-cell functions by limiting mTORC 1 activity and subsequent cellular metabolism.
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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.