Journal article
Metabolic and functional reprogramming of myeloid-derived suppressor cells and their therapeutic control in glioblastoma
Cell Stress, Vol.3(2), pp.47-65
02/01/2019
DOI: 10.15698/cst2019.02.176
PMCID: PMC6551710
PMID: 31225500
Abstract
Glioblastoma, also known as glioblastoma multiforme, is the most common and deadliest form of high-grade malignant brain tumors with limited available treatments. Within the glioblastoma tumor microenvironment (TME), tumor cells, stromal cells, and infiltrating immune cells continuously interact and exchange signals through various secreted factors including cytokines, chemokines, growth factors, and metabolites. Simultaneously, they dynamically reprogram their metabolism according to environmental energy demands such as hypoxia and neo-vascularization. Such metabolic reprogramming can determine fates and functions of tumor cells as well as immune cells. Ultimately, glioma cells in the TME transform immune cells to suppress anti-tumor immune cells such as T, natural killer (NK) cells, and dendritic cells (DC), and evade immune surveillance, and even to promote angiogenesis and tumor metastasis. Glioma-associated microglia/macrophages (GAMM) and myeloid-derived suppressor cells (MDSC) are most abundantly recruited and expanded myeloid lineage cells in glioblastoma TME and mainly lead to immunosuppression. In this review, of myeloid cells we will focus on MDSC as an important driver to induce immunosuppression in glioblastoma. Here, we review current literature on immunosuppressive functions and metabolic reprogramming of MDSCs in glioblastoma and discuss their metabolic pathways as potential therapeutic targets to improve current incurable glioblastoma treatment.
Details
- Title: Subtitle
- Metabolic and functional reprogramming of myeloid-derived suppressor cells and their therapeutic control in glioblastoma
- Creators
- Woong-Jai Won - University of Alabama at BirminghamJessy S. Deshane - University of Alabama at BirminghamJianmei W. Leavenworth - University of Alabama at BirminghamClaudia R. Oliva - University of IowaCorinne E. Griguer - University of Iowa
- Resource Type
- Journal article
- Publication Details
- Cell Stress, Vol.3(2), pp.47-65
- DOI
- 10.15698/cst2019.02.176
- PMID
- 31225500
- PMCID
- PMC6551710
- NLM abbreviation
- Cell Stress
- ISSN
- 2523-0204
- eISSN
- 2523-0204
- Publisher
- Shared Science Publishers Og
- Number of pages
- 19
- Grant note
- P30 DK079626 / NIDDK NIH HHS; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK) P30 CA086862; R01 CA160821 / NCI NIH HHS; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Cancer Institute (NCI) R21 NS100054 / NINDS NIH HHS; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Neurological Disorders & Stroke (NINDS)
- Language
- English
- Date published
- 02/01/2019
- Academic Unit
- Radiation Oncology
- Record Identifier
- 9984312969802771
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