4.7 Review

Lipid Metabolism in Glioblastoma: From De Novo Synthesis to Storage

Journal

BIOMEDICINES
Volume 10, Issue 8, Pages -

Publisher

MDPI
DOI: 10.3390/biomedicines10081943

Keywords

glioblastoma; fatty acids; cholesterol; lipid droplets; SREBP-1; DGAT1; SOAT1; lipotoxicity

Funding

  1. National Institute of Neurological Disorders and Stroke (NINDS)
  2. National Cancer Institute (NCI) of United States [R01NS104332, R01NS112935, R01CA227874, R01CA240726]
  3. American Cancer Society (United States) [RSG-14-228-01-CSM]
  4. OSUCCC-Pelotonia (United States) Idea
  5. Urban and Shelly Meyer Foundation
  6. OSUCCC start-up funds

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This review summarizes the recent progress in understanding lipid metabolism regulation in GBM and discusses novel strategies to induce lipotoxicity in tumor cells by disrupting lipid storage. These findings provide new directions for treating GBM.
Glioblastoma (GBM) is the most lethal primary brain tumor. With limited therapeutic options, novel therapies are desperately needed. Recent studies have shown that GBM acquires large amounts of lipids for rapid growth through activation of sterol regulatory element-binding protein 1 (SREBP-1), a master transcription factor that regulates fatty acid and cholesterol synthesis, and cholesterol uptake. Interestingly, GBM cells divert substantial quantities of lipids into lipid droplets (LDs), a specific storage organelle for neutral lipids, to prevent lipotoxicity by increasing the expression of diacylglycerol acyltransferase 1 (DGAT1) and sterol-O-acyltransferase 1 (SOAT1), which convert excess fatty acids and cholesterol to triacylglycerol and cholesteryl esters, respectively. In this review, we will summarize recent progress on our understanding of lipid metabolism regulation in GBM to promote tumor growth and discuss novel strategies to specifically induce lipotoxicity to tumor cells through disrupting lipid storage, a promising new avenue for treating GBM.

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