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Coculture Assays to Study Macrophage and Microglia Stimulation of Glioblastoma Invasion
Published on: October 20, 2016
Context-Dependent Glioblastoma-Macrophage/Microglia Symbiosis and Associated Mechanisms
Wenjing Xuan1, Maciej S Lesniak1, Charles David James1
1Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Abstract:
Glioblastoma (GBM) is a lethal form of primary brain tumor in human adults. The impact of tumor-intrinsic alterations is not exclusively confined to cancer cells but can also be extended to the tumor microenvironment (TME). Glioblastoma-associated macrophages/microglia (GAMs) are a prominent type of immune cells that account for up to 50% of total cells in GBM. Emerging evidence suggests that context-dependent GBM-GAM symbiotic interactions are pivotal for tumor growth and progression. Here, we discuss how specific genetic alterations in GBM cells affect GAM biology and, reciprocally, how GAMs support GBM progression. We hypothesize that understanding context-dependent GBM-GAM symbiosis may reveal the molecular basis of GBM tumorigenesis and lead to novel candidate treatment approaches aiming to improve GBM patient outcomes.
Insights
Glioblastoma (GBM) cells and their associated immune cells, glioblastoma-associated macrophages/microglia (GAMs), engage in symbiotic interactions that drive tumor growth. Understanding this GBM-GAM relationship may lead to new treatments for brain tumors.
Area of Science:
- Neuro-oncology
- Cancer immunology
- Tumor microenvironment
Background:
- Glioblastoma (GBM) is an aggressive primary brain tumor in adults.
- Tumor-intrinsic alterations in GBM impact the tumor microenvironment (TME).
- Glioblastoma-associated macrophages/microglia (GAMs) are key immune cells within the GBM TME, comprising up to 50% of tumor cells.
Purpose of the Study:
- To discuss the reciprocal interactions between GBM cells and GAMs.
- To explore how genetic alterations in GBM affect GAM biology.
- To elucidate how GAMs contribute to GBM progression.
Main Methods:
- Literature review and synthesis of current research on GBM-GAM interactions.
- Analysis of the impact of genetic alterations in GBM on GAM phenotype and function.
- Examination of the mechanisms by which GAMs promote GBM growth and progression.
Main Results:
- GBM cells influence GAM polarization and function.
- GAMs exhibit pro-tumorigenic activities, including promoting angiogenesis, invasion, and immune suppression.
- Context-dependent symbiotic interactions between GBM and GAMs are crucial for tumor progression.
Conclusions:
- Understanding the intricate GBM-GAM symbiosis is essential for deciphering GBM tumorigenesis.
- Targeting GBM-GAM interactions presents a promising therapeutic strategy for improving patient outcomes.
- Further research into the molecular basis of this symbiosis could reveal novel treatment targets.

