ArticleCancer immunology, immunotherapy : CII2024
DNA hypo-methylation and expression of GBP4 induces T cell exhaustion in pancreatic cancer.
Article in Cancer immunology, immunotherapy : CII, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Guanylate-binding protein 2 (GBP2) drives pancreatic cancer cell proliferation by promoting cell cycle progression via the SP1/SKP2/P27 axis.Journal of translational medicine · 2026Article
- Genome-wide DNA methylation profiling of triple-negative breast cancer uncovers epigenetic biomarkers of tumor identity and the immune microenvironment.NPJ breast cancer · 2026Article
- Epigenetic orchestration of cancer-immune dynamics: mechanisms, technologies, and clinical advancements.Journal of advanced research · 2026Review
- Epigenetic modulation to overcome immune suppression in pancreatic cancer.Clinical epigenetics · 2026Review
- GBP2 condensates promote ferroptosis to sensitize anti-PD-L1 immunotherapy in melanoma.Nature communications · 2025Article
- Integrated transcriptome and single-cell RNA sequencing analysis revealed the prognostic significance of GBP4 in pancreatic adenocarcinoma.Translational oncology · 2025Article
- Article
- Multifaceted Roles of Guanylate-Binding Proteins in Cancer.International journal of molecular sciences · 2025Review
- Postnatal epigenetic differences in calves following transient fetal infection with bovine viral diarrhea virus.BMC genomics · 2025Article
- Epigenetic regulation of CD8Frontiers in immunology · 2025Review
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Authors and funding
12 authors.
Funding
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Abstract
Immunotherapy for pancreatic ductal carcinoma (PDAC) remains disappointing due to the repressive tumor microenvironment and T cell exhaustion, in which the roles of interferon-stimulated genes were largely unknown. Here, we focused on a typical interferon-stimulated gene, GBP4, and investigated its potential diagnostic and therapeutic value in pancreatic cancer. Expression analysis on both local samples and public databases indicated that GBP4 was one of the most dominant GBP family members present in the PDAC microenvironment, and the expression level of GBP4 was negatively associated with patient survival. We then identified DNA hypo-methylation in regulatory regions of GBP4 in PDAC, and validated its regulatory role on GBP4 expression via performing targeted methylation using dCas9-SunTag-DNMAT3A-sgRNA-targeted methylation system on selected DNA locus. After that, we investigated the downstream functions of GBP4, and chemotaxis assays indicated that GBP4 overexpression significantly improved the infiltration of CD8
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