ArticleCell death and differentiation2026
Disruption of RBPJ in liver cancer-infiltrating T cells enhances antitumor immunity through remodeling epigenetic landscape.
Article in Cell death and differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Metabolic cell death: ferroptosis, cuproptosis, and disulfidptosis as a unified framework for targeting metabolic vulnerabilities in disease.Apoptosis : an international journal on programmed cell death · 2026Review
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Authors and funding
11 authors.
Funding
Abstract
Though inhibiting the RBPJ transcription complex reduces PD-L1 expression and alleviates T cell dysfunction in hepatocellular carcinoma (HCC), the tumor immunomodulatory function of RBPJ in T cells is unclear. This study used patient-derived xenograft models to illustrate the role of RBPJ disruption in clinical outcomes and sensitivity to immunotherapy. Immunoprecipitation was performed to identify whether HUWE1 is the E3 ubiquitin ligase for RBPJ. CUT&Tag, ChIP-/ATAC-qPCR, flow cytometry, and CyTOF were used to investigate the molecular mechanism of how RBPJ regulated the function of HCC-infiltrating T cells. Mice with conditional knockout or knock-in of Huwe1 or Rbpj in T cells were used to evaluate their role in the tumor growth. Furthermore, virtual screening, molecular dynamics simulation, immunoprecipitation, and DNA pull-down assays revealed the role of acarbose in RBPJ transcription complex. Our study found that RBPJ expression rose in exhausted T cells, aggravating their exhaustion. Mechanistically, HUWE1 facilitated the K341 ubiquitination of RBPJ through K48 linkage. RBPJ contributed to T cell exhaustion by enhancing the transcription of exhaustion-related genes as a transcription factor, recruiting RUVBL1 to elevate H3K4me3 levels on the promoters of exhaustion-related genes or H3K27ac on their enhancers, and induced the transcription of the KMT2C, thereby increasing H3K4me1 levels on the enhancers of exhaustion-related genes. Furthermore, acarbose-induced damage in the RBPJ transcriptional complex indicated that targeting T cell exhaustion may be a promising HCC treatment. Collectively, our research results indicated that inhibiting the RBPJ in T cells changed the tumor microenvironment from "cold" to "hot".
Identifiers
42562885What OpenQuestion 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 OpenQuestion graph.