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The ERK and JNK pathways in the regulation of metabolic reprogramming

机译:ERK和JNK途径在调节代谢重编程

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摘要

Most tumor cells reprogram their glucose metabolism as a result of mutations in oncogenes and tumor suppressors, leading to the constitutive activation of signaling pathways involved in cell growth. This metabolic reprogramming, known as aerobic glycolysis or the Warburg effect, allows tumor cells to sustain their fast proliferation and evade apoptosis. Interfering with oncogenic signaling pathways that regulate the Warburg effect in cancer cells has therefore become an attractive anti-cancer strategy. However, evidence for the occurrence of the Warburg effect in physiological processes has also been documented. As such, close consideration of which signaling pathways are beneficial targets and the effect of their inhibition on physiological processes are essential. The MAPK/ERK and MAPK/JNK pathways, crucial for normal cellular responses to extracellular stimuli, have recently emerged as key regulators of the Warburg effect during tumorigenesis and normal cellular functions. In this review, we summarize our current understanding of the roles of the ERK and JNK pathways in controlling the Warburg effect in cancer, and discuss their implication in controlling this metabolic reprogramming in physiological processes and opportunities for targeting their downstream effectors for therapeutic purposes.
机译:大多数肿瘤细胞作为癌肠和肿瘤抑制剂中的突变重新编程其葡萄糖代谢,导致细胞生长中涉及的信号传导途径的组成型活化。这种代谢重编程,被称为有氧糖酵解或Warburg效应,允许肿瘤细胞维持其快速增殖和避免细胞凋亡。因此干扰调节癌细胞中的Warburg效应的致癌信号通路已成为一种有吸引力的抗癌策略。但是,还记录了生理过程中发生Warburg效应的证据。因此,密切考虑哪些信号通路是有益的目标,并且它们对生理过程的抑制作用是必不可少的。 MAPK / ERK和MAPK / JNK途径对于细胞外刺激的正常细胞反应至关重要,最近被出现为Warburg效应的关键调节因子,在肿瘤发生和正常的细胞功能期间。在这篇综述中,我们总结了我们目前对ERK和JNK途径在控制癌症中的Warburg效应方面的作用的理解,并探讨了他们在治疗生理过程中的这种代谢重编程的暗示,用于治疗其下游效应的机会。

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