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MicroRNA-661 modulates redox and metabolic homeostasis in colon cancer.

MicroRNA-661 modulates redox and metabolic homeostasis in colon cancer.
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Gómez de Cedrón M, Acín Pérez R, Sánchez-Martínez R, Molina S, Herranz J, Feliu J, Reglero G, Enríquez JA, Ramírez de Molina A,


Gómez de Cedrón M, Acín Pérez R, Sánchez-Martínez R, Molina S, Herranz J, Feliu J, Reglero G, Enríquez JA, Ramírez de Molina A, (click to view)

Gómez de Cedrón M, Acín Pérez R, Sánchez-Martínez R, Molina S, Herranz J, Feliu J, Reglero G, Enríquez JA, Ramírez de Molina A,

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Molecular oncology 2017 10 05() doi 10.1002/1878-0261.12142
Abstract

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. miR661 induces a global increase in reactive oxygen species (ROS), specifically in mitochondrial superoxide anions (SO(-) ), which appears to be mediated by decreased carbohydrate metabolism and pentose phosphate pathway, and by a higher dependency on mitochondrial respiration. miR661 overexpression in non-metastatic human CC cells induces an epithelial-to-mesenchymal transition (EMT) 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 (H6PD) and pyruvate kinase M2 (PKM2) 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.

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