ArticleFrontiers in immunology2025
TGF-β-driven NK Cells plasticity in hepatocellular carcinoma.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Nur77 agonism invigorates Natural Killer cell immunity against hepatocellular carcinoma.Nature communications · 2026Article
- Unveiling the Intricate Dance: Signaling Pathways in Liver Cancer Metabolism and Immunity.Current oncology reports · 2026Review
- Engineering Bi-Specific CAR-NK Cells to Restore Antibody-Dependent Cellular Cytotoxicity in Solid Tumors.Cells · 2026Article
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Authors and funding
16 authors.
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Abstract
Background: Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality, with limited curative options for advanced disease. Natural Killer (NK) cells are critical innate immune effectors, but their anti-tumor function is severely compromised by the immunosuppressive tumor immune microenvironment (TIME), particularly through transforming growth factor-beta (TGF-β). This study investigates the pivotal role of TGF-β signaling in modulating NK cell phenotypes and functions within the HCC TIME. Methods: to comprehensively assess TGF-β pathway activation and its impact on NK cells, tumor-infiltrating lymphocytes (TILs) and liver-infiltrating lymphocytes (LILs) were isolated from HCC patients undergoing curative resection. Phenotypic and functional analyses were performed, along with functional restoration experiments targeting TGF-β signaling. Results: Tumor-infiltrating NK cells (TINKs) exhibited significant activation of both canonical (SMAD-dependent) and non-canonical (TAK1/p38 MAPK) TGF-β signaling, with a predominance of the non-canonical pathway. This activation was associated with the emergence of an ILC1-like NK subset (CD103 Discussion: our findings suggest that while non-canonical TGF-β signaling drives phenotypic reprogramming and contributes to NK cell dysfunction, canonical SMAD-dependent signaling remains a key therapeutic target for functional restoration. These results highlight the dual role of TGF-β in immune modulation and suggest that targeted pathway inhibition could enhance innate anti-tumor responses, opening new avenues for combination therapies in HCC.
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