Metabolism and epigenetics: drivers of tumor cell plasticity and treatment outcomes

被引:8
作者
Gantner, Benjamin N. [1 ]
Palma, Flavio R. [2 ,3 ]
Pandkar, Madhura R. [2 ,3 ]
Sakiyama, Marcelo J. [2 ,3 ]
Arango, Daniel [4 ]
Denicola, Gina M. [5 ]
Gomes, Ana P. [6 ]
Bonini, Marcelo G. [2 ,3 ]
机构
[1] Med Coll Wisconsin, Dept Med, Milwaukee, WI USA
[2] Northwestern Univ, Feinberg Sch Med, Dept Med, Chicago, IL 60611 USA
[3] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Chicago, IL 60611 USA
[4] Northwestern Univ, Feinberg Sch Med, Dept Pharmacol, Chicago, IL USA
[5] H Lee Moffitt Canc Ctr & Res Inst, Dept Metab & Physiol, Tampa, FL USA
[6] H Lee Moffitt Canc Ctr & Res Inst, Dept Mol Oncol, Tampa, FL USA
关键词
GENE-EXPRESSION; TRANSFERRIN RECEPTOR; HISTONE METHYLATION; CANCER-CELLS; TCA CYCLE; IRON; DEHYDROGENASE; INHIBITION; CHROMATIN; FUMARATE;
D O I
10.1016/j.trecan.2024.08.005
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Emerging evidence indicates that metabolism not only is a source of energy and biomaterials for cell division but also acts as a driver of cancer cell plasticity and treatment resistance. This is because metabolic changes lead to remodeling of chromatin and reprogramming of gene expression patterns, furthering tumor cell phenotypic transitions. Therefore, the crosstalk between metabolism and epigenetics seems to hold immense potential for the discovery of novel therapeutic targets for various aggressive tumors. Here, we highlight recent discoveries supporting the concept that the cooperation between metabolism and epigenetics enables cancer to overcome mounting treatment-induced pressures. We discuss how specific metabolites contribute to cancer cell resilience and provide perspective on how simultaneously targeting these key forces could produce synergistic therapeutic effects to improve treatment outcomes.
引用
收藏
页码:992 / 1008
页数:17
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