表观遗传学
生物
癌症
细胞代谢
细胞信号
后生
癌细胞
信号转导
脂质代谢
恶性转化
计算生物学
生物信息学
神经科学
细胞
癌症研究
细胞生物学
遗传学
DNA甲基化
生物化学
基因
基因表达
标识
DOI:10.1016/j.tem.2017.11.003
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.
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