Interacting Cancer Machineries: Cell Signaling, Lipid Metabolism, and Epigenetics

被引:61
作者
Grunt, Thomas W. [1 ,2 ,3 ]
机构
[1] Med Univ Vienna, Div Oncol, Dept Med 1, Signaling Networks Program, Vienna, Austria
[2] Med Univ Vienna, Comprehens Canc Ctr, Vienna, Austria
[3] Med Univ Vienna, Ludwig Boltzmann Cluster Oncol, Vienna, Austria
关键词
FATTY-ACID SYNTHASE; GROWTH-FACTOR-I; ENDOPLASMIC-RETICULUM STRESS; ACETYL-COA CARBOXYLASE; DE-NOVO LIPOGENESIS; ATP-CITRATE LYASE; BREAST-CANCER; PROSTATE-CANCER; OVARIAN-CANCER; HISTONE ACETYLATION;
D O I
10.1016/j.tem.2017.11.003
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Cancer-specific perturbations of signaling, metabolism, and epigenetics can be a cause and/or consequence of malignant transformation. Evidence indicates that these regulatory systems interact with each other to form highly flexible and robust cybernetic networks that promote malignant growth and confer treatment resistance. Deciphering these plexuses using holistic approaches known from systems biology can be instructive for the future design of novel anticancer strategies. In this review, I discuss novel findings elucidating the multiple molecular interdependence among cancer-specific signaling, cell metabolism, and epigenetics to provide an insightful understanding of how major cancer machineries interact with each other during cancer development and progression, and how this knowledge may be used for future co-targeting strategies.
引用
收藏
页码:86 / 98
页数:13
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