ArticleClinical and experimental immunology2021
Down-regulation of PR/SET domain 10 underlies natural killer cell dysfunction in hepatocellular carcinoma.
Article in Clinical and experimental immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 5 citations in OpenAlex.
- Natural killer cell-based therapy for hepatocellular carcinoma (HCC): A literature review.Medical oncology (Northwood, London, England) · 2026Review
- Nutritional Components and Bioactive Substances of Colored Rice: From Molecular Formation, Nutritional and Health Benefits to Industrial Application Prospects.Molecules (Basel, Switzerland) · 2026Review
- Targeting the TIGIT/CD155-induced metabolic checkpoint in NK cells restores anti-tumor immunity and suppresses hepatocellular carcinoma growth.Frontiers in immunology · 2026Article
- Molecular evolution of the transcription factor PRDM genes and expression profiles in response to stimulations and spinal cord injury repair in lamprey (Lethenteron reissneri).Immunogenetics · 2025Article
- Machine learning identification of NK cell immune characteristics in hepatocellular carcinoma based on single-cell sequencing and bulk RNA sequencing.Genes & genomics · 2025Article
- The synergistic interaction landscape of chromatin regulators reveals their epigenetic regulation mechanisms across five cancer cell lines.Computational and structural biotechnology journal · 2022Article
- Down-regulation of PR/SET domain 10 underlies natural killer cell dysfunction in hepatocellular carcinoma.Clinical and experimental immunology · 2021Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
Hepatocellular carcinoma (HCC) is the world's leading cause of tumor-related mortalities. Natural killer (NK) cells play a critical role at the first immunological defense line against HCC initiation and progression. NK cell dysfunction is therefore an important mechanism for immune evasion of HCC cells. In the present study using a murine HCC model, we revealed the down-regulation of PR/SET Domain 10 (PRDM10) in hepatic NK cells that were phenotypically and functionally exhausted. PRDM10 silencing diminished the expression of natural killer group 2 member D (NKG2D) and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), augmented T cell immunoglobulin and ITIM domain (TIGIT) expression, and decreased the expression of interferon (IFN)-γ, perforin and granzyme B in normal hepatic NK cells in vitro. Consistently, PRDM10-deficient NK cells exhibited impaired cytotoxicity on target cells. In contrast, PRDM10 over-expression promoted NKG2D and Fas ligand (FasL) expression, reduced CD96 expression and enhanced transcripts of IFN-γ, perforin and granzyme B in NK cells in vivo. Moreover, PRDM10 silencing and PRDM10 over-expression down-regulated and up-regulated Eomesodermin (Eomes) expression, respectively. In summary, this study reveals PRDM10 down-regulation as a novel mechanism underlying NK cell dysfunction and identifies PRDM10 as a supporting factor of NK cell function.
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