1. Sodium channel γENaC mediates IL-17 synergized high salt induced inflammatory stress in breast cancer cells.
- Author
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Amara S, Ivy MT, Myles EL, and Tiriveedhi V
- Subjects
- Blotting, Western, Breast Neoplasms physiopathology, Carcinogens pharmacology, Cell Line, Tumor, Enzyme-Linked Immunosorbent Assay, Epithelial Sodium Channels genetics, Female, Humans, Stress, Physiological genetics, Up-Regulation drug effects, Breast Neoplasms immunology, Epithelial Sodium Channels metabolism, Inflammation, Interleukin-17 metabolism, Sodium Chloride pharmacology, Stress, Physiological immunology
- Abstract
Chronic inflammation is known to play a critical role in the development of cancer. Recent evidence suggests that high salt in the tissue microenvironment induces chronic inflammatory milieu. In this report, using three breast cancer-related cell lines, we determined the molecular basis of the potential synergistic inflammatory effect of sodium chloride (NaCl) with interleukin-17 (IL-17). Combined treatment of high NaCl (0.15M) with sub-effective IL-17 (0.1 nM) induced enhanced growth in breast cancer cells along with activation of reactive nitrogen and oxygen (RNS/ROS) species known to promote cancer. Similar effect was not observed with equi-molar mannitol. This enhanced of ROS/RNS activity correlates with upregulation of γENaC an inflammatory sodium channel. The similar culture conditions have also induced expression of pro-inflammatory cytokines such as IL-6, TNFα etc. Taken together, these data suggest that high NaCl in the cellular microenvironment induces a γENaC mediated chronic inflammatory response with a potential pro-carcinogenic effect., (Copyright © 2015 Elsevier Inc. All rights reserved.)
- Published
- 2016
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