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Modulation of Mammary Stromal Cell Lactate Dynamics by Ambient Glucose and Epithelial Factors
Author(s) -
Tobar Nicolas,
Porras Omar,
Smith Patricio C.,
Barros L. Felipe,
Martínez Jorge
Publication year - 2017
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.25398
Subject(s) - stromal cell , cell culture , motility , biology , glycolysis , glucose transporter , glucose uptake , epithelium , carbohydrate metabolism , stroma , cell , warburg effect , microbiology and biotechnology , chemistry , medicine , endocrinology , metabolism , biochemistry , cancer research , insulin , immunology , genetics , immunohistochemistry
Hyperglycemia is a risk factor for a variety of human cancers. Increased access to glucose and that tumor metabolize glucose by a glycolytic process even in the presence of oxygen (Warburg effect), provide a framework to analyze a particular set of metabolic adaptation mechanisms that may explain this phenomenon. In the present work, using a mammary stromal cell line derived from healthy tissue that was subjected to a long‐term culture in low (5 mM) or high (25 mM) glucose, we analyzed kinetic parameters of lactate transport using a FRET biosensor. Our results indicate that the glucose pre‐culture and soluble epithelial factors constitute a stimulus for lactate stromal production, factors that also modify the kinetic parameters and the monocarboxylate transporters expression in stromal cells. We also observed a vectorial flux of lactate from stroma to epithelial cells in a co‐culture setting and found that the uptake of lactate by epithelial cells correlates with the degree of malignancy. Glucose preconditioning of the stromal cell stimulated epithelial motility. Our findings suggest that lactate generated by stromal cells in the high glucose condition stimulate epithelial migration. Overall, our results support the notion that glucose not only provides a substrate for tumor nutrition but also behaves as a signal promoting malignancy. J. Cell. Physiol. 232: 136–144, 2017. © 2016 Wiley Periodicals, Inc.