Abstract
ABSTRACTMetabolic reprogramming is now well established as one of the hallmarks of cancer. The renewed interest in this topic has spurred a remarkable advance in our understanding of the metabolic alterations in cancer cells and in the tumour microenvironment. Initially, this research focussed on identifying the metabolic processes that provided cancer cells with building blocks for growth or to prevent oxidative damage and death. In addition to providing detailed insight into the mechanisms by which oncogenic signalling pathways modulate metabolic processes, this research also revealed multiple nodes within the metabolic network that can be targeted for the selective elimination of cancer cells. However, recent years have seen a paradigm shift in the field of cancer metabolism; while early studies focussed mainly on the metabolic processes within a cancer cell, recent approaches also consider the impact of metabolic cross-talk between different cell types within the tumour or study cancer within the organismal metabolic context. The Review articles presented in this themed Special Collection of Disease Models & Mechanisms aim to provide an overview of the recent advances in the field. The Collection also contains research articles that describe how metabolic inhibition can improve the efficacy of targeted therapy and introduce a new zebrafish model to study metabolic tumour-host interactions. We also present ‘A model for life’ interviews: a new interview with Karen Vousden and a previously published one with Lewis Cantley that provide insight into these two leaders' personal scientific journeys that resulted in seminal discoveries in the field of cancer metabolism. In this Editorial, we summarise some of the key insights obtained from studying cancer metabolism. We also describe some of the many exciting developments in the field and discuss its future challenges.
Highlights
Altered glucose metabolism in cancer cells was discovered almost 100 years ago, when Otto Warburg demonstrated that tumours, instead of fully oxidising glucose to CO2, switch to aerobic glycolysis and ferment glucose to lactate (Warburg, 1924)
It is clear that the signals derived by oncogenes or tumour suppressors intersect with the metabolic network on multiple levels to drive the production of macromolecules for cancer cell growth and proliferation (Deberardinis et al, 2008)
Lung cancer cells cultured in vitro displayed metabolic features of aerobic glycolysis and glutamine-dependent anaplerosis, while tumours generated by genetic induction of Kras or by implantation of murine or human lung cancer cells showed higher levels of oxidative glucose metabolism and no entry of glutamine into the tricarboxylic acid (TCA) cycle (Davidson et al, 2016)
Summary
Altered glucose metabolism in cancer cells was discovered almost 100 years ago, when Otto Warburg demonstrated that tumours, instead of fully oxidising glucose to CO2, switch to aerobic glycolysis and ferment glucose to lactate (Warburg, 1924). One of these strategies is metabolic competition, by which cancer cells deplete essential nutrients, such as glucose, from the tumour microenvironment and thereby prevent the activation of cytotoxic T cells (Chang et al, 2015).
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