2026-06-14T02:28:12Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/106322025-06-13T10:32:32Zcom_20.500.12105_15322com_20.500.12105_2051com_20.500.12105_2052col_20.500.12105_16977col_20.500.12105_19617

00925njm 22002777a 4500 dc Gutiérrez-Salmerón, María author García-Martínez, José Manuel author Martínez-Useros, Javier author Fernández-Aceñero, María Jesús author Viollet, Benoit author Olivier, Severine author Chauhan, Jagat author Chocarro-Calvo, Ana author García-Jiménez, Custodia author De la Vieja, Antonio author Lucena, Silvia R. author Goding, Colin R. author 2020-06 Coordination of gene expression with nutrient availability supports proliferation and homeostasis and is shaped by protein acetylation. Yet how physiological/pathological signals link acetylation to specific gene expression programs and whether such responses are cell-type-specific is unclear. AMP-activated protein kinase (AMPK) is a key energy sensor, activated by glucose limitation to resolve nutrient supply-demand imbalances, critical for diabetes and cancer. Unexpectedly, we show here that, in gastrointestinal cancer cells, glucose activates AMPK to selectively induce EP300, but not CREB-binding protein (CBP). Consequently, EP300 is redirected away from nuclear receptors that promote differentiation towards β-catenin, a driver of proliferation and colorectal tumorigenesis. Importantly, blocking glycogen synthesis permits reactive oxygen species (ROS) accumulation and AMPK activation in response to glucose in previously nonresponsive cells. Notably, glycogen content and activity of the ROS/AMPK/EP300/β-catenin axis are opposite in healthy versus tumor sections. Glycogen content reduction from healthy to tumor tissue may explain AMPK switching from tumor suppressor to activator during tumor evolution. PLoS Biol. 2020 Jun 30;18(6):e3000732. 10.1371/journal.pbio.3000732 1545-7885 PLoS biology 32603375 http://hdl.handle.net/20.500.12105/10632 Paradoxical activation of AMPK by glucose drives selective EP300 activity in colorectal cancer