期刊
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
卷 636, 期 -, 页码 110-122出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.abb.2017.08.009
关键词
Glut1; Chemoresistance; Triple-negative breast cancer
资金
- NRF from the Korea Research Foundation [2016R1A2B4011196]
- National Research Foundation of Korea [2016R1A2B4011196] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Cancer cells require increased aerobic glycolysis to support rapid cell proliferation. For their increased energy demands, cancer cells express glucose transporter (Glut) proteins at a high level. Glut1 is associated with basal-like breast cancer and is considered a potential therapeutic target. To investigate the possibility of Glut1 as a therapeutic target in breast cancer cells, we downregulated Glut1 in triple negative breast cancer (TNBC) cell lines using a short hairpin system. We determined whether Glut1 silencing might enhance anti-proliferative effect of chemotherapeutic agents. Contrary to our hypothesis, ablation of Glut1 attenuated apoptosis and increased drug resistance via upregulation of p-Akt/p-GSK-3 beta (Ser9)/beta-cateninisurvivin. These results indicated that the potential of Glut1 as a therapeutic target should be carefully reevaluated. (C) 2017 Published by Elsevier Inc.
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