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Related Experiment Video

Updated: Jan 8, 2026

Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis
07:45

Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis

Published on: November 28, 2015

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Metabolic-transcriptional rewiring by NFE2L2 promotes M2 macrophage polarization and anti-PD-L1 resistance in glioma.

Qiusi Tian1, Qun Zhang2, Rongzhen Deng3

  • 1Department of Neurosurgery, 3201 Hospital, Hanzhong, 723001, China.

Cancer Cell International
|December 12, 2025
PubMed
Summary

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This summary is machine-generated.

Nuclear factor erythroid 2-related factor 2 (NFE2L2) is overexpressed in glioma, promoting tumor growth and immune suppression. Targeting NFE2L2 reshapes the tumor microenvironment, enhancing immunotherapy response and suppressing glioma progression.

Area of Science:

  • Neuro-oncology
  • Immunology
  • Molecular Biology

Background:

  • Glioma exhibits an immunosuppressive microenvironment linked to poor prognosis.
  • The transcription factor NFE2L2's role in glioma remains unclear.

Purpose of the Study:

  • Investigate the regulatory role and molecular mechanisms of NFE2L2 in glioma.
  • Determine NFE2L2's impact on the tumor immune microenvironment and therapeutic response.

Main Methods:

  • TCGA database and clinical sample analysis.
  • In vitro M2-like macrophage polarization model.
  • NFE2L2 overexpression and deficiency mouse models.
  • Transcriptomic and metabolomic analyses.

Main Results:

Keywords:
GliomaMetabolomeNFE2L2Tumor-associated macrophages

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Last Updated: Jan 8, 2026

Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis
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Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
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Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages

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  • NFE2L2 is overexpressed in glioma, correlating with M2-like TAM infiltration.
  • NFE2L2 enhances glioma cell migration and invasion.
  • NFE2L2 deficiency improves immunotherapy response and suppresses tumor progression.
  • NFE2L2 promotes M2-like macrophage polarization and modulates the tumor microenvironment.

Conclusions:

  • NFE2L2 plays a critical role in glioma development and immune evasion.
  • NFE2L2 is a potential therapeutic target for glioma immunotherapy.