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Related Experiment Video

Updated: May 30, 2025

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells

Published on: November 28, 2015

Characterization of NOD-like receptor-based molecular heterogeneity in glioma and its association with immune

Chunlin Lu¹, Huihao Ma¹, Jie Wang²

¹Department of Neurosurgery, First Affiliated Hospital of Dalian Medical University, Dalian, China.

Frontiers in Immunology

|January 30, 2025

Summary

NOD-like receptor (NLR) signaling impacts glioblastoma (GBM) by influencing its subtypes, immune microenvironment, and metabolism. The TRIP6 gene is identified as a key player in GBM progression, offering potential therapeutic targets.

Keywords:

GBM NLR pathway TRIP6 clinical heterogeneity immune microenvironment metabolism reprogramming

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Last Updated: May 30, 2025

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells

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Published on: November 28, 2015

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Published on: July 31, 2017

Digital Spatial Profiling for Characterization of the Microenvironment in Adult-Type Diffusely Infiltrating Glioma

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Published on: September 13, 2022

Area of Science:

Immunology
Oncology
Molecular Biology

Background:

The role of NOD-like receptor (NLR) signaling in high-grade gliomas, particularly glioblastoma (GBM), remains incompletely understood.
Understanding NLR's influence on GBM heterogeneity is crucial for developing targeted therapies.

Purpose of the Study:

To investigate the association between NLR signaling and clinical heterogeneity in GBM patients.
To explore the function of NLR pathway hub genes in GBM development and progression.

Main Methods:

Transcriptomic data from 496 GBM patients were analyzed using NMF clustering based on NLR gene expression.
Pathway activity, immune microenvironment, and prognostic markers were assessed.
LASSO and COX regression identified key prognostic genes, with TRIP6 further investigated via molecular biology experiments.

Main Results:

GBM patients were classified into two subtypes (C1, C2) with distinct clinical outcomes, immune, and metabolic profiles based on NLR expression.
A prognostic marker with high AUC (0.601-0.846) was developed.
TRIP6 was identified as a crucial NLR hub gene, overexpressed in GBM, and its knockdown inhibited GBM cell proliferation and migration.

Conclusions:

The NLR signaling pathway significantly regulates the GBM immune microenvironment and metabolic reprogramming.
TRIP6 emerges as a potential key gene in the NLR pathway, influencing GBM's malignant behavior and representing a therapeutic target.