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Tumor cells impair immunological synapse formation via central nervous system-enriched metabolite

Yihong Li1, Min Huang1, Minger Wang2

  • 1Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou 510120, China.

Cancer Cell
|May 31, 2024
PubMed

Insights

Tumors evade immune surveillance by mimicking the central nervous system (CNS). Overexpressed N-acetyltransferase 8-like (NAT8L) and its metabolite N-acetylaspartate (NAA) impair anti-tumor immunity by inhibiting natural killer (NK) and CD8+ T cells.

Area of Science:

  • Immunology
  • Neuroscience
  • Oncology

Background:

  • Tumors utilize immune evasion strategies.
  • The central nervous system (CNS) possesses inherent immune-restraining features.
  • It remains unclear if tumors and the CNS share immunosuppressive mechanisms.

Purpose of the Study:

  • To investigate whether tumors share immunosuppressive programs with the CNS.
  • To identify molecular mechanisms by which tumors evade immune surveillance.

Main Methods:

  • Multi-omics data analysis of HER2+ breast cancer patient tumors treated with trastuzumab and anti-PD-L1.
  • Investigated the role of N-acetyltransferase 8-like (NAT8L) and N-acetylaspartate (NAA) in tumor immunosuppression.

Main Results:

  • CNS-enriched NAT8L and its metabolite NAA were overexpressed in resistant tumors.
  • NAA impairs anti-tumor immunity by inhibiting natural killer (NK) and CD8+ T cell cytotoxicity.
  • NAA disrupts immunological synapse formation by affecting lamin A acetylation, inhibiting lytic granule polarization.

Conclusions:

  • Tumor cells mimic CNS anti-inflammatory mechanisms to evade anti-tumor immunity.
  • NAT8L is a potential therapeutic target to enhance anti-cancer agent efficacy.
Keywords:
Tumor metabolismanti-tumor immunityimmune checkpoint blockadeimmunological synapseneuroinflammation

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