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Peer-reviewedCC BY 4.0Frontiers in Immunology

TRIM14 recruits BRCC3 to stabilize PD-L1 by suppressing p62-dependent selective autophagy in glioma

  • Yan Wu1,2
  • Xujun Wang2
  • Mengqiu Li2
  • Rong Wang2
  • Yaoxing Wu1,2,3
  • Di Liu2,4
4 affiliations
  1. 1Institute of Precision Medicine, the First Affiliated Hospital, Sun Yat-sen University
  2. 2MOE Key Laboratory of Gene Function and Regulation, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University
  3. 3Department of Critical Care Medicine, The First Affiliated Hospital of Sun Yat-sen University, Sun Yat-sen University
  4. 4Organ Transplant Center, The First Affiliated Hospital, Sun Yat-sen University
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Abstract

Glioma remains largely refractory to immune-checkpoint blockade, in part because tumor-intrinsic mechanisms sustain programmed death-ligand 1 (PD-L1) and reinforce an immunosuppressive microenvironment. Tripartite motif-containing 14 (TRIM14) is an immune associated protein. However, the role of TRIM14 in PD-L1 homeostasis in glioma is incompletely defined. Here we reported that TRIM14 was increased in malignancies and was particularly associated with overall survival in glioma. Single-nucleus analysis showed that TRIM14-positive nuclei were predominantly malignant, indicating association between TRIM14 and glioma progression. We also found TRIM14 upregulated PD-L1 protein levels without materially changing CD274 mRNA in glioma cells. Additionally, knockout of TRIM14 reduced tumor growth in vivo . Mechanistically, TRIM14 recruits deubiquitinase BRCC3 to reduce K63-linked ubiquitination of PD-L1 in glioma cells, thereby inhibiting p62-mediated autophagic degradation of PD-L1. This pathway prompts that TRIM14 or BRCC3 maybe candidate targets for therapeutic intervention in glioma.

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Cite

BibTeXRIS
BibTeX
@article{wu2026trim14,
  title = {{TRIM14 recruits BRCC3 to stabilize PD-L1 by suppressing p62-dependent selective autophagy in glioma}},
  author = {Yan Wu and Xujun Wang and Mengqiu Li and Rong Wang and Yaoxing Wu and Di Liu},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1942769},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1942769/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - TRIM14 recruits BRCC3 to stabilize PD-L1 by suppressing p62-dependent selective autophagy in glioma
AU  - Yan Wu
AU  - Xujun Wang
AU  - Mengqiu Li
AU  - Rong Wang
AU  - Yaoxing Wu
AU  - Di Liu
PY  - 2026
DA  - 2026/10/13
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1942769
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1942769/full
AB  - Glioma remains largely refractory to immune-checkpoint blockade, in part because tumor-intrinsic mechanisms sustain programmed death-ligand 1 (PD-L1) and reinforce an immunosuppressive microenvironment. Tripartite motif-containing 14 (TRIM14) is an immune associated protein. However, the role of TRIM14 in PD-L1 homeostasis in glioma is incompletely defined. Here we reported that TRIM14 was increased in malignancies and was particularly associated with overall survival in glioma. Single-nucleus analysis showed that TRIM14-positive nuclei were predominantly malignant, indicating association between TRIM14 and glioma progression. We also found TRIM14 upregulated PD-L1 protein levels without materially changing CD274 mRNA in glioma cells. Additionally, knockout of TRIM14 reduced tumor growth in vivo . Mechanistically, TRIM14 recruits deubiquitinase BRCC3 to reduce K63-linked ubiquitination of PD-L1 in glioma cells, thereby inhibiting p62-mediated autophagic degradation of PD-L1. This pathway prompts that TRIM14 or BRCC3 maybe candidate targets for therapeutic intervention in glioma.
SN  - 1664-3224
ER  -