Dataset for: MicroRNA-661 modulates redox and metabolic homeostasis in Colon Cancer

Cancer cell survival and metastasis are dependent on a metabolic reprogramming able to increase 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-), that seems 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 cells metabolism is also compromised upon miR661 overexpression. We propose hexose 6 phosphate dehydrogenase (H6PD) and pyruvate kinase M2 (PKM2) as two 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.