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BATF2 is a glutamine-responsive tumour suppressor required for type-I interferon-dependent anti-tumour immunity

Wang Gong1,2, Hülya F Taner3, Yuesong Wu4

  • 1Department of Head and Neck Surgery, the University of Texas M.D. Anderson Cancer Center, Houston, TX, USA.

Nature Communications
|December 28, 2025
PubMed

Insights

Glutamine inhibits the tumor suppressor BATF2 in head and neck cancers, promoting immune escape. Restoring BATF2 enhances anti-tumor immunity and controls cancer progression.

Area of Science:

  • Oncology
  • Immunology
  • Metabolic pathways

Background:

  • Tumor suppressors are crucial in cancer, but some are inhibited by metabolic cues rather than mutation.
  • Head and Neck Squamous Cell Carcinomas (HNSCC) present unique challenges in cancer treatment.

Purpose of the Study:

  • To identify and characterize a novel tumor suppressor, BATF2, in HNSCC.
  • To elucidate the role of metabolic cues, specifically glutamine, in regulating BATF2 expression and function.
  • To investigate the impact of BATF2 on anti-tumor immunity and cancer progression.

Main Methods:

  • Epigenetic analysis to determine BATF2 silencing mechanisms.
  • Correlation studies between BATF2 expression, interferon signatures, and STING pathway activation.
  • Metabolic profiling and dietary interventions (glutamine-rich diet).
  • In vivo studies using syngeneic, orthotopic, and carcinogen-induced HNSCC models.
  • Analysis of immune cell infiltration (CD206+, CD8+ T-cells) and T-cell exhaustion markers.

Main Results:

  • BATF2 is epigenetically silenced by glutamine in HNSCC.
  • BATF2 expression correlates strongly with type-I interferon and Th1 signatures, and its phosphorylation promotes STING oligomerization.
  • High glutamine levels or BATF2 deficiency lead to unfavorable metabolic profiles for type-I interferon production and impair STING-mediated tumor control.
  • Cancer cell-specific BATF2 expression promotes T-cell effector function, reduces exhaustion, and induces HNSCC rejection.
  • Host Batf2 deficiency accelerates cancer initiation by increasing CD206+ myeloid cells and decreasing effector CD8+ T-cells.

Conclusions:

  • BATF2 acts as a tumor suppressor in HNSCC, with its loss mediated by metabolic cues in the tumor microenvironment (TME).
  • Metabolic dysregulation of BATF2 contributes to cancer immune escape.
  • Targeting BATF2 or modulating glutamine metabolism may offer novel therapeutic strategies for HNSCC.

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