Lipidized glioblastoma: A rare differentiation pattern

Gupta, Kirti; I, Kalra; Salunke, Pravin; Vasishta, Rakesh Kumar

doi:10.1111/j.1440-1789.2010.01141.x

Cited by 14 publications

(6 citation statements)

References 11 publications

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“…LDs are commonly viewed as energy storage organelles since the TAGs stored in LDs can readily be hydrolyzed into free FAs and glycerol for energy production by patatin-like phospholipase domain-containing protein 2 (PNPLA2), a member of the PNPLA family, also known as adipose triglyceride lipase (ATGL) 18 and monoacylglycerol lipase (MAGL) 14 . In the central nervous system, LD levels are barely detectable, however, recent studies show that neurons and glia accumulate LDs under disease conditions such as brain tumors 19,20 .…”

Section: Introductionmentioning

confidence: 99%

Lipid accumulation and oxidation in glioblastoma multiforme

Taïb

Aboussalah

Moniruzzaman

et al. 2019

Sci Rep

101

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Glioblastoma multiforme (GBM) is the most common and lethal primary malignant brain tumor in adults. Despite the multimodal standard treatments for GBM, the median survival is still about one year. Analysis of brain tissues from GBM patients shows that lipid droplets are highly enriched in tumor tissues while undetectable in normal brain tissues, yet the identity and functions of lipid species in GBM are not well understood. The aims of the present work are to determine how GBM utilizes fatty acids, and assess their roles in GBM proliferation. Treatment of U138 GBM cells with a monounsaturated fatty acid, oleic acid, induces accumulation of perilipin 2-coated lipid droplets containing triglycerides enriched in C18:1 fatty acid, and increases fatty acid oxidation. Interestingly, oleic acid also increases glucose utilization and proliferation of GBM cells. In contrast, pharmacologic inhibition of monoacylglycerol lipase attenuates GBM proliferation. Our findings demonstrate that monounsaturated fatty acids promote GBM proliferation via triglyceride metabolism, suggesting a novel lipid droplet-mediated pathway which may be targeted for GBM treatment.

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Section: Introductionmentioning

confidence: 99%

Lipid accumulation and oxidation in glioblastoma multiforme

Taïb

Aboussalah

Moniruzzaman

et al. 2019

Sci Rep

101

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“…In cancers such as glioblastoma multiforme, enhanced fatty acid storage and synthesis provide the necessary resources for survival and rapid proliferation [1]. Although otherwise highly heterogeneous, most cancer types present a lipogenic phenotype characterized by the upregulation of key enzymes and transcriptional factors controlling lipid metabolism (e.g.…”

Section: Introductionmentioning

confidence: 99%

Pharmacological inhibition of lipid droplet formation enhances the effectiveness of curcumin in glioblastoma

Zhang

Cui

Amiri

et al. 2016

European Journal of Pharmaceutics and Biopharmaceutics

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a b s t r a c tIncreased lipid droplet number and fatty acid synthesis allow glioblastoma multiforme, the most common and aggressive type of brain cancer, to withstand accelerated metabolic rates and resist therapeutic treatments. Lipid droplets are postulated to sequester hydrophobic therapeutic agents, thereby reducing drug effectiveness. We hypothesized that the inhibition of lipid droplet accumulation in glioblastoma cells using pyrrolidine-2, a cytoplasmic phospholipase A2 alpha inhibitor, can sensitize cancer cells to the killing effect of curcumin, a promising anticancer agent isolated from the turmeric spice. We observed that curcumin localized in the lipid droplets of human U251N glioblastoma cells. Reduction of lipid droplet number using pyrrolidine-2 drastically enhanced the therapeutic effect of curcumin in both 2D and 3D glioblastoma cell models. The mode of cell death involved was found to be mediated by caspase-3. Comparatively, the current clinical chemotherapeutic standard, temozolomide, was significantly less effective in inducing glioblastoma cell death. Together, our results suggest that the inhibition of lipid droplet accumulation is an effective way to enhance the chemotherapeutic effect of curcumin against glioblastoma multiforme.

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“…Malignant gliomas with heavily lipidized (foamy) tumor cells were initially described by Kepes and Rubinstein 12 in 1981 and later reported by other authors 15–21 . Histologically, almost all tumor cells were noted to have vacuolated foamy cytoplasm or rarely adipocyte‐like differentiation, 17 increased pleomorphism, numerous mitotic figures, mild endothelial proliferation of the blood vessels, and necrosis with pseudopallisading of the tumor cells.…”

Section: Discussionmentioning

confidence: 94%

Lipidized glioblastoma: Pathological and molecular characteristics

Singh¹,

Iftinca

Easaw³

2012

Neuropathology

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We report a rare case of a 33-year-old man with a lipidized glioblastoma multiforme (GBM) in the right posterior frontal region. Histologically the tumor had all the typical features of a GBM but with the rare observation of lipidized differentiation. There were multiple mitoses, extensive vascular proliferation, focal necrosis and the tumor cells had abundant xanthomatous cytoplasm and marked nuclear pleomorphism. The tumor showed immunoreactivity with GFAP. The O(6) - methylguanine methyltransferase (MGMT) promoter was methylated and there were no isocitrate dehydrogenase (IDH)1 and IDH2 mutations. To the best of our knowledge, this is the first time MGMT promoter status and IDH mutation assessment have been reported in a case of lipidized GBM.

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Lipidized glioblastoma: A rare differentiation pattern

Cited by 14 publications

References 11 publications

Lipid accumulation and oxidation in glioblastoma multiforme

Lipid accumulation and oxidation in glioblastoma multiforme

Pharmacological inhibition of lipid droplet formation enhances the effectiveness of curcumin in glioblastoma

Lipidized glioblastoma: Pathological and molecular characteristics

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