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The Tumor Microenvironment

The Tumor Microenvironment

Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...

The Tumor Microenvironment

The Tumor Microenvironment

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Related Experiment Video

Updated: Apr 18, 2026

Preparation Of Neovascular Tissues from Human Glioma Tissues for Quantitative Proteomics Analysis of Tumor Angiogenesis

Preparation Of Neovascular Tissues from Human Glioma Tissues for Quantitative Proteomics Analysis of Tumor Angiogenesis

Published on: March 20, 2026

Targeting Tumour Microtubes to Disrupt Glioma Networks.

Jeremy Rich^1,2,3, Tengfei Huang^1,2,3, Po Zhang^2,3

¹Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA.

Research Square

|April 17, 2026

Summary

This summary is machine-generated.

Glioma stem cells form communication networks via tumor microtubes (TMs). Targeting FASTKD2 disrupts TM communication, inhibiting glioma growth and enhancing therapy efficacy.

Keywords:

cancer neuroscience glioblastoma glioma stem cells local protein synthesis tumor microtubes tumor network

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Published on: February 24, 2021

Area of Science:

Neuroscience
Cancer Biology
Mitochondrial Biology

Background:

Glioma cells form multicellular networks using tumor microtubes (TMs).
TMs facilitate tumor-tumor and neuron-tumor connectivity, promoting growth and therapy resistance.
Molecular mechanisms and therapeutic targets for TMs remain largely unknown.

Purpose of the Study:

Investigate the molecular regulation of TMs in glioma.
Identify potential therapeutic strategies targeting TM-mediated communication.
Explore the role of localized protein synthesis in TM function.

Main Methods:

Proteomics and functional screening of TMs.
Analysis of FASTKD2's role in mitochondrial RNA metabolism.
Structure-function screening of linezolid's effects on TM communication.

Main Results:

Glioma stem cells (GSCs) preferentially form TMs, which locally synthesize neurotransmitter receptors and metabolic enzymes.
FASTKD2, an inner mitochondrial component, is crucial for local protein synthesis within TMs.
Targeting FASTKD2 disrupts TM network communication and tumor proliferation by affecting mitochondrial RNA metabolism.
The antibiotic linezolid inhibits FASTKD2-mitochondrial RNA interactions, disrupting TM communication and enhancing anti-cancer therapy.

Conclusions:

Glioma cells utilize neuronal-like mechanisms, including localized protein synthesis, to enhance TM-mediated network communication.
Disruption of FASTKD2-mediated mitochondrial RNA metabolism represents a novel therapeutic vulnerability in gliomas.
Targeting TM communication with agents like linezolid can overcome therapy resistance and improve treatment outcomes.