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. 2018 Aug 16;8:12252. doi: 10.1038/s41598-018-29708-9

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Feedback regulation circuit of metabolic phenotypes and miR-342-3p expression. (a) Graphical representation of the relation between miR-342-3p, MCT1 and lactate consumption in tumoral cells. TN tumors maintain a homeostatic relation between glycolytic and oxidative cells: glycolytic cells produce lactate as a bio-product, which is then exported to the medium through MCT transporters and used as an energetic source by oxidative cells, which incorporate it through MCT1 and convert it into pyruvate to then metabolize it via mitochondria. When miR-342-3p is over-expressed, it negatively regulates the expression of MCT1 disrupting the lactate fluxes, mainly the incorporation of lactate into the oxidative cells, promoting a metabolic change to a glycolytic state and establishing a competition for glucose. (b) Graphical representation of the hypothesized relation between the over-expression of miR-342-3p and metabolic states in the glycolytic MDAMB468 cells. The up-modulation of miR-342-3p expression in a glycolytic cell line model produces an accumulation of extracellular lactate by the inhibition of the lactate transporter MCT1, accompanied by an increment of intracellular lactate, while glucose presents a lower concentration in the transfected cells, together with a decrease of the redox ratio. A reduction in the number of oxidative cells and consequently an increment of glycolytic cells also occurred. (c) Immunoblots of MCT1 protein expression in MDAMB468 cells cultured under hypoxic conditions and glucose starvation or not after 24, 48 and 72 hr. Densitometric analysis is indicated as percentage in the blot. Plot figure is a group of blots cropped from different parts of the same gel, complete and original blots are shown in Sup Fig 4. qRT-PCR evaluation of (d) MCT1, (e) miR-342-3p and (f) miR-210 expression in MDAMB468 cells cultured in hypoxic conditions and under glucose starvation or not during 24, 48 and 72 hr. Results are representative of three independent experiments with three technical replicates, each summarized as the geometric mean +/− standard deviation error.