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Review
. 2017 Nov 1:408:174-181.
doi: 10.1016/j.canlet.2017.07.014. Epub 2017 Jul 22.

Metabolic regulation of glioma stem-like cells in the tumor micro-environment

Tom M Thomas  1 , John S Yu  2
Affiliations
Review

Metabolic regulation of glioma stem-like cells in the tumor micro-environment

Tom M Thomas et al. Cancer Lett. .

Abstract

Cancer metabolism has emerged as one of the most interesting old ideas being revisited from a new perspective. In the early 20th century Otto Warburg declared metabolism the prime cause in a disease of many secondary causes, and this statement seems more prescient in view of modern expositions into the true nature of tumor evolution. As the complexity of tumor heterogeneity becomes more clear from a genetic perspective, it is important to consider the inevitably heterogeneous metabolic components of the tumor and the tumor microenvironment. High grade gliomas remain one of the most difficult to treat solid tumors, due in part to the highly vascularized nature of the tumor and the maintenance of more resistant stem-like subpopulations within the tumor. Maintenance of glioma stem cells (GSCs) requires specific alterations within the cells and the greater tumor microenvironment with regards to signaling and metabolism. Specific niches within gliomas help foster the survival of stem-like sub-populations of cells with high tumorigenicity and high metabolic plasticity. Understanding these maintenance pathways and the metabolic dependencies within the niche may highlight potential avenues of addressing tumor resistance and recurrence in glioma patients.

Keywords: Cancer metabolism; Cancer stem cells; Glioblastoma; Glioma stem cells; Microenvironment.

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Conflict of interest statement

8 Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Cancer stem cell hypothesis continues to evolve. (A) traditional cancer stem cell hypothesis suggested hierarchal model where only certain stem-like cell (red) retained capacity to repopulate a tumor and drive continued tumor progression, (B) the clonal model of stem cell propagation suggests many cells within the tumor retains this stem-like repopulation capacity, (C) the newest models suggest a hybrid model that allows for dedifferentiation and transdifferentiation within a tumor from multiple stem precursors in response to intra- and extratumoral pressures, driving tumor recurrence and heterogeneity
Figure 2
Figure 2
Cancer stem cell metabolism may demonstrate another element of cellular plasticity that provides a basis for therapeutic resistance and tumor recurrence after treatment interventions. More terminally differentiated tumor cells may not be as metabolically flexible as stem cells that can switch to different metabolic pathways and different fuel sources more readily.
Figure 3
Figure 3
Interplay between tumor metabolism and the tumor microenvironment as well as its effect on the cancer stem cell compartment is vital to properly understanding the complex dynamics of tumor progression and recurrence
See this image and copyright information in PMC

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