Abstract
Lipid metabolism reprogramming plays important role in cell growth, proliferation, angiogenesis and invasion in cancers. However, the diverse lipid metabolism programmes and prognostic value during glioma progression remain unclear. Here, the lipid metabolism‐related genes were profiled using RNA sequencing data from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) database. Gene ontology (GO) and gene set enrichment analysis (GSEA) found that glioblastoma (GBM) mainly exhibited enrichment of glycosphingolipid metabolic progress, whereas lower grade gliomas (LGGs) showed enrichment of phosphatidylinositol metabolic progress. According to the differential genes of lipid metabolism between LGG and GBM, we developed a nine‐gene set using Cox proportional hazards model with elastic net penalty, and the CGGA cohort was used for validation data set. Survival analysis revealed that the obtained gene set could differentiate the outcome of low‐ and high‐risk patients in both cohorts. Meanwhile, multivariate Cox regression analysis indicated that this signature was a significantly independent prognostic factor in diffuse gliomas. Gene ontology and GSEA showed that high‐risk cases were associated with phenotypes of cell division and immune response. Collectively, our findings provided a new sight on lipid metabolism in diffuse gliomas.
Highlights
Metabolic reprogramming has been recognized as a new hallmark of cancer cells.[1]
It has reported that unsaturated fatty acid, cholesterol esters and phosphatidylcholine are only present in high‐ grade gliomas through magnetic resonance spectroscopy (NMR)
Our results indicated a strong connection between patients' survival and lipid metabolism in diffuse glioma
Summary
Metabolic reprogramming has been recognized as a new hallmark of cancer cells.[1]. Proliferative cancer cells can acquire lipids by enhancing lipid uptake, lipolysis and de novo fatty acid synthesis.[4]. Glioma is one of the most treatment‐refractory cancers and highly resistant to chemo and radiotherapy.[5] Most diffuse LGGs and most glioblastomas will eventually recur and often trans‐ form into a higher grade. Offer et al found that extracel‐ lular lipid loading augments hypoxic paracrine signalling and pro‐ motes glioma angiogenesis and macrophage infiltration.[8] GPIHBP1, a GDP‐anchored protein of capillary endothelial cells, facilitated tri‐ glyceride‐rich lipoproteins (TRLs) processing and provided a source of lipid nutrients for glioma cells.[9] Marifia and colleagues revealed that sphingosine‐1‐phosphate (S1P) fuelled proliferative and stem‐ ness qualities of glioblastoma stem cells.[10] the distinct lipid metabolism programmes and prognostic value in glioma progression need further study. We profiled the lipid metabolism status in 859 diffuse glioma samples with gene expression data from TCGA and CGGA database. Our results indicated a strong connection between patients' survival and lipid metabolism in diffuse glioma
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