ArticleThe EMBO journal2023
Antitumor T-cell function requires CPEB4-mediated adaptation to chronic endoplasmic reticulum stress.
Article in The EMBO journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 15 citations in OpenAlex.
- SNAP23 regulates CPEB4 in the autophagy of hepatocellular carcinoma.Scientific reports · 2026Article
- RNA-binding proteins and ribonucleoproteins as determinants of immunity.Nature reviews. Immunology · 2026Review
- Posttranscriptional reprogramming controls MASLD progression through chronic ER stress adaptation.Science advances · 2026Article
- Stress-Induced Down-Regulation of CPEB4 Disrupts Sodium Channel Regulation and Myocardial Excitability.JACC. Basic to translational science · 2026Article
- Identification and validation of an endoplasmic reticulum stress related model to predict prognosis and tumor microenvironment in neuroblastoma.BMC cancer · 2026Article
- Targeting organelle function in T cells for cancer immunotherapy.Nature reviews. Immunology · 2026Review
- LncRNA EWSAT1 promotes colorectal cancer progression by regulating the miR-330-5p/CPEB4 axis.American journal of translational research · 2026Article
- Single-cell signaling network profiling during redox stress reveals dynamic redox regulation in immune cells.Nature communications · 2025Article
- CD4 T cell dysfunction is associated with bacterial recrudescence during chronic tuberculosis.Nature communications · 2025Article
- CPEB4 modulates liver cancer progression by translationally regulating hepcidin expression and sensitivity to ferroptosis.JHEP reports : innovation in hepatology · 2025Article
- Cytoplasmic regulation of the poly(A) tail length as a potential therapeutic target.RNA (New York, N.Y.) · 2025Review
- CD4 T cell dysfunction is associated with bacterial recrudescence during chronic tuberculosis.bioRxiv : the preprint server for biology · 2025Article
- ER-associated degradation adapter Sel1L is required for CD8Cell reports · 2024Article
- circKDM1A suppresses bladder cancer progression by sponging miR-889-3p/CPEB3 and stabilizing p53 mRNA.iScience · 2024Article
- Navigating the landscape of the unfolded protein response in CD8Frontiers in immunology · 2024Review
- Antitumor T-cell function requires CPEB4-mediated adaptation to chronic endoplasmic reticulum stress.The EMBO journal · 2023Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor growth is influenced by a complex network of interactions between multiple cell types in the tumor microenvironment (TME). These constrained conditions trigger the endoplasmic reticulum (ER) stress response, which extensively reprograms mRNA translation. When uncontrolled over time, chronic ER stress impairs the antitumor effector function of CD8 T lymphocytes. How cells promote adaptation to chronic stress in the TME without the detrimental effects of the terminal unfolded protein response (UPR) is unknown. Here, we find that, in effector CD8 T lymphocytes, RNA-binding protein CPEB4 constitutes a new branch of the UPR that allows cells to adapt to sustained ER stress, yet remains decoupled from the terminal UPR. ER stress, induced during CD8 T-cell activation and effector function, triggers CPEB4 expression. CPEB4 then mediates chronic stress adaptation to maintain cellular fitness, allowing effector molecule production and cytotoxic activity. Accordingly, this branch of the UPR is required for the antitumor effector function of T lymphocytes, and its disruption in these cells exacerbates tumor growth.
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What Socratic holds
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 Socratic graph.