1. 3B, a novel photosensitizer, inhibits glycolysis and inflammation via miR-155-5p and breaks the JAK/STAT3/SOCS1 feedback loop in human breast cancer cells.
- Author
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Lei K, Du W, Lin S, Yang L, Xu Y, Gao Y, Xu B, Tan S, Xu Y, Qian X, Liang X, and Liu J
- Subjects
- Adenosine Triphosphate metabolism, Base Sequence, Breast Neoplasms genetics, Cell Line, Tumor, Female, Gene Expression Regulation, Neoplastic drug effects, Glucose, Heterocyclic Compounds, 4 or More Rings chemistry, Humans, Janus Kinases metabolism, L-Lactate Dehydrogenase metabolism, Lactic Acid metabolism, Models, Biological, Photosensitizing Agents chemistry, STAT3 Transcription Factor metabolism, Suppressor of Cytokine Signaling Proteins metabolism, Breast Neoplasms pathology, Feedback, Physiological drug effects, Glycolysis drug effects, Heterocyclic Compounds, 4 or More Rings pharmacology, Inflammation pathology, MicroRNAs metabolism, Photosensitizing Agents pharmacology, Signal Transduction
- Abstract
Compared to normal cells, most cancer cells produce ATP by glycolysis under aerobic conditions rather than via the tricarboxylic acid cycle (TCA). This study is intended to determine whether 3B, a novel photosensitizer, can inhibit glycolysis and inflammation in breast cancer cells. We showed that 3B had the ability to repress glucose consumption as well as the generation of ATP, lactate and lactate dehydrogenase. 3B-PDT not only inhibited the expression of IL-1β and IL-6 but also affected the JAK-STAT3 inflammatory pathway in vitro. The present study showed that 3B featured a significant inhibitory effect on the expression of microRNA-155-5p and SOCS1 might serve as a target gene. In vivo studies revealed that 3B inhibited tumor growth and exhibited almost no side effects. Therefore, through the anti-glycolytic effect and breakage of the JAK/STAT3/SOCS1 feedback loop via miR-155-5p, 3B may potentially serve as a potential therapeutic agent against breast cancer., (Copyright © 2016 Elsevier Masson SAS. All rights reserved.)
- Published
- 2016
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