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Updated: Jun 23, 2026

Genetic Profiling and Genome-Scale Dropout Screening to Identify Therapeutic Targets in Mouse Models of Malignant Peripheral Nerve Sheath Tumor
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Genetic Profiling and Genome-Scale Dropout Screening to Identify Therapeutic Targets in Mouse Models of Malignant Peripheral Nerve Sheath Tumor

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PCK2 as a potential therapeutic target for aggressive MYC-amplified non-WNT/non-SHH medulloblastoma based on tumor

Shuaishuai Xue1,2, Zhengming Zhan1, Yonghua Cai1

  • 1Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou north road 1838, Guangzhou, 510515, Guangdong Provincial, China.

Acta Neuropathologica Communications
|June 21, 2026
PubMed

Insights

This study identifies PCK2 as a key driver in aggressive medulloblastoma, linking metabolic reprogramming and immune microenvironment. Targeting PCK2 may offer new therapeutic strategies for pediatric brain tumors.

Area of Science:

  • Pediatric Oncology
  • Cancer Metabolism
  • Tumor Immunology

Background:

  • Medulloblastoma, a common pediatric posterior fossa tumor, shows metabolic reprogramming and immune microenvironment heterogeneity in non-WNT/non-SHH subtypes.
  • The interplay between metabolic reprogramming and tumor immune microenvironment (TIME) in these aggressive medulloblastoma subtypes is not well understood.

Purpose of the Study:

  • To identify molecular features and potential therapeutic targets in non-WNT/non-SHH medulloblastoma.
  • To investigate the link between metabolic reprogramming and the tumor immune microenvironment in aggressive medulloblastoma.

Main Methods:

  • Integrated transcriptomic data from public databases (GEO, EMBL-EBI) for non-WNT/non-SHH medulloblastoma.
  • Analyzed the Grp3/4 transcriptional continuum to identify key genes.
  • Utilized short hairpin RNA (shRNA) knockdown experiments in MYC-amplified medulloblastoma cells to validate gene function.

Main Results:

  • Identified PCK2, a key gene in the TCA cycle, as highly correlated with the Grp3/4 transcriptional continuum score.
  • Validated PCK2 as a driver of proliferation, migration, invasion, and glycolysis in medulloblastoma cells.
  • Demonstrated PCK2's role in promoting M2 macrophage polarization, suggesting metabolic-TIME crosstalk.

Conclusions:

  • Metabolic-TIME crosstalk is a significant prognostic determinant in aggressive medulloblastoma subtypes.
  • PCK2 is a potential therapeutic target for aggressive medulloblastoma, offering insights for precision therapy strategies.
Keywords:
Immune MicroenvironmentMedulloblastomaMetabolismPCK2non-WNT/non-SHH

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