Fructose-induced metabolic reprogramming of cancer cells

被引:4
|
作者
Ting, Kenneth K. Y. [1 ,2 ]
机构
[1] Univ Toronto, Dept Immunol, Toronto, ON, Canada
[2] Univ Hlth Network, Toronto Gen Hosp Res Inst, Toronto, ON, Canada
来源
FRONTIERS IN IMMUNOLOGY | 2024年 / 15卷
基金
加拿大健康研究院;
关键词
fructose; cancer; metabolic reprogramming; tumor microenvironment (TME); ketohexokinase (KHK); GLUT5; metabolism; glycolysis; DIETARY FRUCTOSE; CORN SYRUP; GLUCOSE; TRANSPORTER; GLUT2; EXPRESSION; RESISTANCE; PHENOTYPE; DRIVES;
D O I
10.3389/fimmu.2024.1375461
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Excess dietary fructose consumption has been long proposed as a culprit for the world-wide increase of incidence in metabolic disorders and cancer within the past decades. Understanding that cancer cells can gradually accumulate metabolic mutations in the tumor microenvironment, where glucose is often depleted, this raises the possibility that fructose can be utilized by cancer cells as an alternative source of carbon. Indeed, recent research has increasingly identified various mechanisms that show how cancer cells can metabolize fructose to support their proliferating and migrating needs. In light of this growing interest, this review will summarize the recent advances in understanding how fructose can metabolically reprogram different types of cancer cells, as well as how these metabolic adaptations can positively support cancer cells development and malignancy.
引用
收藏
页数:7
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