Silencing of Glut1 induces chemoresistance via modulation of Akt/GSK-3β/β-catenin/survivin signaling pathway in breast cancer cells

Sunhwa Oh, Hyungjoo Kim, Kee Soo Nam, Incheol Shin

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

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-3β (Ser9)/β-catenin/survivin. These results indicated that the potential of Glut1 as a therapeutic target should be carefully reevaluated.

Original languageEnglish
Pages (from-to)110-122
Number of pages13
JournalArchives of Biochemistry and Biophysics
Volume636
DOIs
StatePublished - 2017 Dec 15

Keywords

  • Chemoresistance
  • Glut1
  • Triple-negative breast cancer

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