Editorial: Cell stress, metabolic reprogramming, and cancer

The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis (1). Mitochondria, beyond being the site of aerobic respiration, are at the crossroads of a variety of metabolic and signaling pathways resulting key regulatory organelles in cell life and death decision. Thus, it is no surprise that genomic, functional, and structural mitochondrial alterations have been associated with cancer and that mitochondria have become a pharmacological target in cancer therapy (2). Proliferating tumor cells show increased glycolysis and convert the majority of glucose to l-lactate, even in normoxic conditions. This is known as the Warburg effect. Actually, in many tumors, mitochondria are not defective in oxidative phosphorylation, and in the last decade, the molecular basis of Warburg effect has been reconsidered in the context of a set of concerted changes in energy metabolism and mitochondrial function that support tumorigenesis. This process, referred to as reprogramming of energy metabolism, is an emerging hallmark of cancer development (3, 4). This Research Topic presents one review, five mini-reviews, and an opinion article on the achievements and perspectives of studies on important aspects of cancer cell metabolic reprogramming whose mechanisms and regulation are still largely elusive. It also sheds light on certain novel functional components, which rewires cell metabolism in tumor transformation.