Giulia Santinon

TL;DR: Findings suggest that aerobic glycolysis endows cancer cells with particular metabolic properties and at the same time sustains transcription factors with potent pro‐tumorigenic activities such as YAP/TAZ.

TL;DR: Current data linking YAP/TAZ to metabolism is discussed and it is suggested how this coupling might coordinate nutrient availability with genetic programs that sustain tissue growth, neoplastic cell proliferation, and tumor malignancy.

TL;DR: A general mechanism centered on Lipin-1 and SREBP is identified that links the physical cell microenvironment to a key metabolic pathway and contributes to the pro-survival activity of ROCK inhibitors in pluripotent stem cells.

TL;DR: It is shown that sublethal concentrations of different compounds that decrease mitochondrial ATP production specifically downregulate Wnt/β-catenin signaling in vitro in colon cancer cells and in–vivo in zebrafish reporter lines.

TL;DR: YAP/TAZ couples cell proliferation with a metabolism suited for DNA replication and facilitates escape from oncogene‐induced senescence, and this study indicates that this activity might be relevant during the initial phases of tumour progression or during experimental stem cell reprogramming induced by YAP.