Metabolic reprogramming in glioblastoma: the influence of cancer metabolism on epigenetics and unanswered questions

被引:224
作者
Agnihotri, Sameer [1 ]
Zadeh, Gelareh [1 ,2 ]
机构
[1] Univ Hlth Network, Princess Margaret Canc Ctr, MacFeeters Hamilton Brain Tumor Ctr, Toronto, ON, Canada
[2] Univ Hlth Network, Toronto Western Hosp, Dept Neurosurg, Toronto, ON, Canada
关键词
epigenetics; metabolic reprogramming; molecular signaling; Warburg effect; PYRUVATE-KINASE M2; ATP-CITRATE LYASE; FATTY-ACID SYNTHASE; INTEGRATED GENOMIC ANALYSIS; LACTIC-ACID; ADJUVANT TEMOZOLOMIDE; AEROBIC GLYCOLYSIS; IDH2; MUTATIONS; HEXOKINASE-II; MOUSE MODELS;
D O I
10.1093/neuonc/nov125
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
A defining hallmark of glioblastoma is altered tumor metabolism. The metabolic shift towards aerobic glycolysis with reprogramming of mitochondrial oxidative phosphorylation, regardless of oxygen availability, is a phenomenon known as the Warburg effect. In addition to the Warburg effect, glioblastoma tumor cells also utilize the tricarboxylic acid cycle/oxidative phosphorylation in a different capacity than normal tissue. Altered metabolic enzymes and their metabolites are oncogenic and not simply a product of tumor proliferation. Here we highlight the advantages of why tumor cells, including glioblastoma cells, require metabolic reprogramming and how tumor metabolism can converge on tumor epigenetics and unanswered questions in the field.
引用
收藏
页码:160 / 172
页数:13
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