2026-06-14T03:31:31Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/72212024-09-27T09:42:16Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Gómez de Cedrón, Marta author Acin-Perez, Rebeca author Sánchez-Martínez, Ruth author Molina, Susana author Herranz, Jesús author Feliu, Jaime author Reglero, Guillermo author Enriquez, Jose Antonio author Ramírez de Molina, Ana author 2017 Cancer cell survival and metastasis are dependent on metabolic reprogramming that is capable of increasing resistance to oxidative and energetic stress. Targeting these two processes can be crucial for cancer progression. Herein, we describe the role of microRNA-661 (miR661) as epigenetic regulator of colon cancer (CC) cell metabolism. MicroR661 induces a global increase in reactive oxygen species, specifically in mitochondrial superoxide anions, which appears to be mediated by decreased carbohydrate metabolism and pentose phosphate pathway, and by a higher dependency on mitochondrial respiration. MicroR661 overexpression in non-metastatic human CC cells induces an epithelial-to-mesenchymal transition phenotype, and a reduced tolerance to metabolic stress. This seems to be a general effect of miR661 in CC, since metastatic CC cell metabolism is also compromised upon miR661 overexpression. We propose hexose-6-phosphate dehydrogenase and pyruvate kinase M2 as two key players related to the observed metabolic reprogramming. Finally, the clinical relevance of miR661 expression levels in stage-II and III CC patients is discussed. In conclusion, we propose miR661 as a potential modulator of redox and metabolic homeostasis in CC. Mol Oncol. 2017; 11(12):1768-1787 10.1002/1878-0261.12142 1878-0261 1574-7891 Molecular oncology 28981199 http://hdl.handle.net/20.500.12105/7221 Bioenergetics Colon cancer Metabolomics miR Oxidative stress MicroRNA-661 modulates redox and metabolic homeostasis in colon cancer