ArticleFrontiers in immunology2022
Targeting Stress Sensor Kinases in Hepatocellular Carcinoma-Infiltrating Human NK Cells as a Novel Immunotherapeutic Strategy for Liver Cancer.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Natural killer cell-based therapy for hepatocellular carcinoma (HCC): A literature review.Medical oncology (Northwood, London, England) · 2026Review
- Targeting the TIGIT/CD155-induced metabolic checkpoint in NK cells restores anti-tumor immunity and suppresses hepatocellular carcinoma growth.Frontiers in immunology · 2026Article
- NK Cell Senescence in Cancer: From Molecular Mechanisms to Therapeutic Opportunities.Aging and disease · 2025Review
- TGF-β-driven NK Cells plasticity in hepatocellular carcinoma.Frontiers in immunology · 2025Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Natural killer (NK) cells may become functionally exhausted entering hepatocellular carcinoma (HCC), and this has been associated with tumor progression and poor clinical outcome. Hypoxia, low nutrients, immunosuppressive cells, and soluble mediators characterize the intratumor microenvironment responsible for the metabolic deregulation of infiltrating immune cells such as NK cells. HCC-infiltrating NK cells from patients undergoing liver resection for HCC were sorted, and genome-wide transcriptome profiling was performed. We have identified a marked general upregulation of gene expression profile along with metabolic impairment of glycolysis, OXPHOS, and autophagy as well as functional defects of NK cells. Targeting p38 kinase, a stress-responsive mitogen-activated protein kinase, we could positively modify the metabolic profile of NK cells with functional restoration in terms of TNF-α production and cytotoxicity. We found a metabolic and functional derangement of HCC-infiltrating NK cells that is part of the immune defects associated with tumor progression and recurrence. NK cell exhaustion due to the hostile tumor microenvironment may be restored with p38 inhibitors with a selective mechanism that is specific for tumor-infiltrating-not affecting liver-infiltrating-NK cells. These results may represent the basis for the development of a new immunotherapeutic strategy to integrate and improve the available treatments for HCC.
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