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The correlation between TRIM28 expression and immune checkpoints in CRPC.

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This study reveals TRIM28

Keywords:
TRIM28anti‐tumor immunitycGAS‐STING pathwaycastration‐resistant prostate cancerimmune checkpointsingle‐cell transcriptome sequencing

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Area of Science:

  • Oncology
  • Immunology
  • Molecular Biology

Background:

  • Castration-resistant prostate cancer (CRPC) remains a significant clinical challenge.
  • The molecular mechanisms underlying immune cell dynamics in CRPC are not fully understood.
  • TRIM28's role in CRPC immunity has not been previously investigated.

Purpose of the Study:

  • To investigate the role and molecular mechanisms of TRIM28 in castration-resistant prostate cancer (CRPC).
  • To explore TRIM28's impact on immune cell populations and function within the CRPC tumor microenvironment.
  • To elucidate TRIM28's potential regulatory role in the cGAS-STING pathway in CRPC.

Main Methods:

  • High-throughput single-cell transcriptome sequencing and bioinformatics analysis.
  • Correlation analysis with The Cancer Genome Atlas (TCGA) data.
  • TRIM28 knockout mouse models, in vitro experiments, and in situ tumor models.

Main Results:

  • Dynamic TRIM28 expression changes were observed in CRPC immune cells (macrophages, CD8+ T cells).
  • TRIM28 knockout suppressed tumor growth, inhibited M2 macrophage polarization, and enhanced CD8+ T cell activity.
  • TRIM28 knockout modulated gene expression linked to the cGAS-STING pathway.

Conclusions:

  • TRIM28 plays a previously unrecognized anti-tumor immune role in CRPC.
  • TRIM28 influences immune cell quantity and function, potentially via the cGAS-STING pathway.
  • Targeting TRIM28 presents a promising therapeutic strategy for CRPC.