Wnt Regulates TERT—Putting the Horse Before the Cart
Menée in vitro et à l'aide d'un modèle murin, cette étude met en évidence un mécanisme par lequel, en régulant l'expression de la télomérase, la voie de signalisation Wnt joue un rôle dans la tumorigenèse
Maintaining the length of telomeres—the ends of chromosomes—is essential for all cells that divide many times. The enzyme telomerase lengthens these ends, counterbalancing their shortening that occurs each time chromosomes are copied. Telomerase is essential for cell viability, and loss of its function from the loss of only one of two copies of the encoding gene can lead to the failure of stem cell renewal that is seen in premature aging conditions such as dyskeratosis congenita, aplastic anemia, and pulmonary fibrosis (1). Conversely, telomerase activity is increased in many cancers and may be required for cancer cells to maintain their telomere length (2). On page 1549 in this issue, Hoffmeyer et al. (3) show that a cell signaling pathway known to play a prominent role in development, stem cell renewal, and cancer (4)—the canonical Wnt pathway—also regulates the expression of telomerase.
Science , commentaire, 2012