ArticleJournal for immunotherapy of cancer2025
TRIM28 drives immune evasion via PARP1 SUMOylation and NAD
Article in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- ROS-ATM-CBP axis-mediated PARP1 lactylation aggravates doxorubicin-induced cardiotoxicity.Clinical and translational medicine · 2026Article
- MT1G promotes the progression of ccRCC by suppressing ferroptosis through activation of the PI3K-AKT pathway.Translational oncology · 2026Article
- TIF1 Family Proteins as Modulators of Cell Death: Mechanisms and Therapeutic Opportunities.Biomolecules · 2026Review
- Editorial: Unraveling renal cell carcinoma: pathogenesis, therapeutic strategies, and future perspectives.Frontiers in medicine · 2026Article
- Integrative analysis of scRNA-seq and bulk RNA-seq with machine learning develops a nucleotide metabolism-based prognostic model for ccRCC and reveals the function of IFI30.Frontiers in oncology · 2026Article
- TRIM family proteins: dual roles in tumor immunity.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImmune checkpoint blockade (ICB) therapy has demonstrated significant clinical potential in a variety of cancers; however, its efficacy in clear cell renal cell carcinoma (ccRCC) remains suboptimal. In ccRCC, an increased infiltration of CD8
methodsTripartite motif-containing 28 (TRIM28) was identified as a potential therapeutic target through single-cell transcriptomics (GSE159115) and Geneformer-based perturbation screening. Functional validation was performed by constructing shTRIM28 and overexpression cell models to assess tumor proliferation, CD8
resultsWe identified TRIM28 as a central regulator of immune evasion in ccRCC. Using high-throughput gene knockout screening, we demonstrated that TRIM28 depletion reprograms malignant epithelial cells toward a less aggressive phenotype and significantly enhances tumor cell susceptibility to cytotoxic T lymphocyte killing. Mechanistically, TRIM28 promotes immune resistance through dual immunometabolic mechanisms: first, by stabilizing PARP1 and promoting its SUMOylation, which in turn amplifies PD-L1 expression via NAD
conclusionsThis study reveals that TRIM28 is a key regulator of PD-L1 expression and T cell dysfunction in ccRCC through PARP1 stabilization and NAD
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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 Socratic graph.