Phosphoenolpyruvate carboxykinase 2 is a promising prognostic biomarker that correlates with peritumoral dendritic cell infiltration in glioblastoma

  • 0Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.

|

|

Summary

This summary is machine-generated.

Phosphoenolpyruvate carboxykinase 2 (PCK2) is upregulated in glioblastoma, indicating a poor prognosis. PCK2 correlates with immune cell infiltration and immunosuppression, suggesting therapeutic potential.

Area Of Science

  • Oncology
  • Molecular Biology
  • Immunology

Background

  • Phosphoenolpyruvate carboxykinase 2 (PCK2) is a molecule of interest in cancer research.
  • Its clinical relevance and biological role in glioblastoma remain largely uninvestigated.
  • Understanding PCK2's function is crucial for developing new glioblastoma therapies.

Purpose Of The Study

  • To investigate the clinical significance of PCK2 in glioblastoma.
  • To explore the association between PCK2 expression and tumor-infiltrating immune cells.
  • To elucidate the role of PCK2 in glioblastoma immunosuppression.

Main Methods

  • Analysis of PCK2 expression in three major glioma cohorts (TCGA, CGGA, Rembrandt).
  • Kaplan-Meier survival analysis, Cox regression, and immunohistochemistry.
  • Gene Set Enrichment Analysis (GSEA), CIBERSORT, and double immunofluorescence for immune cell profiling and co-expression analysis.

Main Results

  • PCK2 expression is elevated in glioblastoma and serves as an independent poor prognostic indicator.
  • PCK2 is significantly associated with the mesenchymal subtype, immune infiltrates, and immunosuppression.
  • PCK2 correlates with dendritic cell infiltration and co-expresses with CD11C and PD-L1 in GBM tissues.

Conclusions

  • PCK2 is a potential therapeutic target for glioblastoma.
  • PCK2-mediated dendritic cell infiltration contributes to glioblastoma immunosuppression.
  • Targeting PCK2 may offer a novel strategy to overcome glioblastoma immune evasion.