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CARD9 deficiency promotes pancreatic cancer growth by blocking dendritic cell maturation via SLC6A8-mediated creatine

Cheng Tian1, Huimin Yuan1, Yi Lu2

  • 1Department of Pharmacology, School of Pharmacy, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Oncoimmunology
|April 24, 2023
PubMed

Insights

Caspase-recruitment domain-containing protein 9 (CARD9) enhances anti-tumor immunity in pancreatic cancer by promoting dendritic cell maturation and function. Loss of CARD9 impairs this immunity, accelerating cancer progression.

Area of Science:

  • Immunology
  • Oncology
  • Metabolism

Background:

  • Pancreatic cancer (PC) has a low survival rate and poor prognosis.
  • Caspase-recruitment domain-containing protein 9 (CARD9) is expressed in innate immune cells and its role in PC is unclear.

Purpose of the Study:

  • To investigate the role of CARD9 in pancreatic cancer progression and anti-tumor immunity.
  • To identify the molecular mechanisms by which CARD9 influences dendritic cell function.

Main Methods:

  • Utilized CARD9-deficient PC mouse models.
  • Assessed dendritic cell (DC) maturation and T cell activation in vivo and in vitro.
  • Analyzed metabolite profiles of DCs and identified key molecular pathways involved in CARD9 signaling.

Main Results:

  • CARD9 deficiency accelerated PC progression and reduced survival rates.
  • CARD9 knockout impaired DC maturation and T cell activation.
  • Creatine levels were decreased in CARD9-deficient DCs due to inhibited SLC6A8 transcription, mediated by the CARD9-BCL10-MALT1 complex and p65 activation.

Conclusions:

  • CARD9 is crucial for maintaining DC function and anti-tumor immunity in pancreatic cancer.
  • CARD9 deficiency promotes PC progression by reducing creatine transport into DCs, leading to DC immaturity and impaired immune response.

Keywords:
CARD9SLC6A8creatinedendritic cellspancreatic cancer

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