Many cells including immune, neuronal, cancer and stem cells become dependent on aerobic glycolysis to escape apoptosis and accommodate their bioenergetics needs. How this metabolic change, also known as the Warburg effect, is regulated remains largely unknown. The Warburg effect has been widely investigated in cancer cells where first it was observed with the aim of decoding the molecular networks controlling its activation for therapeutic purposes. However, in recent years, it has become more evident that this phenotypic trait is also used by normal non- cancerous cells such as immune cells (like lymphocytes) to adapt to the increased energy requirements during cell activation. Moreover, the elevated rate of aerobic glycolysis in the brain provides the biosynthetic support needed for the production of biomass during normal development and during synapse formation following a brain injury. Likewise, aerobic glycolysis is required for vessel sprouting. Yet, it was also shown that enhanced aerobic glycolysis has also a survival role for neurons, protecting them from apoptosis induced by reactive oxygen species (ROS). This latter trait is shared with cancer cells that commonly escape chemotherapeutic treatment. Although the exact mechanisms underlying such metabolic shift in those different cells and tissues is not fully clear, recent works have started to shed light of the common intracellular signaling pathways that make these distinct class of cells not so different from each other.
This Research Topic is intended to discuss and review all the intracellular signaling regulating the Warburg effect in cancerous and normal non-cancerous cells by research articles, mini-reviews and reviews.
cells and the implication for treatment of neurodegenerative disease.
• The metabolic reprogramming in the context of naïve and primed pluripotent states, somatic reprogramming, and hematopoietic and skeletal muscle tissue stem cells, and the implications for regenerative medicine.
• The metabolic regulation in cancer cells escaping apoptosis during treatment.