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This Foreword introduces the nine Review articles in our Focus on Tumour Metabolism and discusses the main areas of tumour metabolism for further research.
Acidosis reprograms the metabolism of cancer cells toward fatty acid oxidation by downregulating acetyl-CoA carboxylase ACC2 through histone deacetylation
Sousaet al. demonstrate a reciprocal metabolic cross-talk between pancreatic stellate cells (PSCs) and pancreatic tumour cells whereby secreted autophagic alanine from PSCs is taken up by tumour cells and used as an alternative carbon source to support tumour growth.
Chaeet al. show that mitochondrially-localized AKT phosphorylates pyruvate dehydrogenase kinase 1 (PDK1) to promote tumour cell growth and survival in hypoxic conditions.
This Review provides an overview of glutamine metabolism and its involvement in tumorigenesisin vitro and in vivo, exploring the recent potential applications of basic science discoveries in the clinical setting.
The reprogramming of glucose metabolism in cancer cells, which have increased flux through glycolysis and related pathways, offers the promise of targeted inhibitors to selectively eradicate cancer cells either by themselves or as adjuvants to existing therapeutic modalities.
Serine supports many biosynthetic pathways, including the one-carbon cycle. This Review discusses how cancer cells acquire and use serine, and explores novel therapeutic approaches to limit serine metabolism.
The availability of oxygen and nutrients changes during tumour evolution, which can have an effect on gene expression and diverse metabolic reactions as cells try to adapt to the new environment. In this Review the authors summarize how these metabolic adaptations are integrated in hypoxic tumour cells and their role in disease progression.