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.

中文翻译：

---

相互作用的癌症机制：细胞信号传导、脂质代谢和表观遗传学

信号、代谢和表观遗传学的癌症特异性扰动可能是恶性转化的原因和/或结果。有证据表明，这些监管系统相互作用，形成高度灵活和强大的控制论网络，促进恶性生长并赋予治疗抵抗力。使用系统生物学中已知的整体方法来破译这些神经丛对于未来新型抗癌策略的设计具有指导意义。在这篇综述中，我讨论了阐明癌症特异性信号、细胞代谢和表观遗传学之间多分子相互依赖性的新发现，以深入了解主要癌症机制在癌症发展和进展过程中如何相互作用，以及这些知识如何发挥作用用于未来的联合定位策略。