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TGF-β-driven NK Cells plasticity in hepatocellular carcinoma.

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Transforming growth factor-beta (TGF-β) impairs Natural Killer (NK) cell anti-tumor function in hepatocellular carcinoma (HCC). Targeting canonical TGF-β signaling restores NK cell function, offering new therapeutic strategies for HCC.

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ILC1-like cellsNK cellsTGF-βfunctional restorationhepatocellular carcinomaimmune function

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Area of Science:

  • Immunology
  • Oncology
  • Molecular Biology

Background:

  • Hepatocellular carcinoma (HCC) is a major cause of cancer mortality with limited treatment options for advanced stages.
  • Natural Killer (NK) cells are crucial for innate immunity but are suppressed within the tumor immune microenvironment (TIME) by factors like transforming growth factor-beta (TGF-β).

Purpose of the Study:

  • To investigate the role of TGF-β signaling in altering NK cell phenotypes and functions within the HCC tumor immune microenvironment.
  • To assess the impact of TGF-β pathway activation on NK cells, tumor-infiltrating lymphocytes (TILs), and liver-infiltrating lymphocytes (LILs) in HCC patients.

Main Methods:

  • Isolation of TILs and LILs from HCC patients undergoing resection.
  • Phenotypic and functional analysis of NK cells.
  • Functional restoration experiments targeting TGF-β signaling pathways.

Main Results:

  • Tumor-infiltrating NK cells (TINKs) showed activation of both canonical (SMAD-dependent) and non-canonical (TAK1/p38 MAPK) TGF-β signaling.
  • A distinct ILC1-like NK subset (CD103+/CD49a+) emerged in tumors, expressing inhibitory receptors, while conventional NK cells (cNKs) were functionally impaired.
  • Blocking TGF-β receptor binding and SMAD3 activation successfully restored cNK functionality.

Conclusions:

  • Non-canonical TGF-β signaling contributes to NK cell dysfunction and phenotypic changes in HCC.
  • Canonical SMAD-dependent TGF-β signaling is a viable therapeutic target for restoring NK cell function.
  • Targeted inhibition of TGF-β pathways may enhance innate anti-tumor immunity, presenting novel combination therapy options for HCC.