Silencing of Glut1 induces chemoresistance via modulation of Akt/GSK-3β/β-catenin/survivin signaling pathway in breast cancer cells
- Authors
- Oh, Sunhwa; Kim, Hyungjoo; Nam, KeeSoo; Shin, Incheol
- Issue Date
- Dec-2017
- Publisher
- ELSEVIER SCIENCE INC
- Keywords
- Glut1; Chemoresistance; Triple-negative breast cancer
- Citation
- ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, v.636, pp.110 - 122
- Indexed
- SCIE
SCOPUS
- Journal Title
- ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS
- Volume
- 636
- Start Page
- 110
- End Page
- 122
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/18605
- DOI
- 10.1016/j.abb.2017.08.009
- ISSN
- 0003-9861
- 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-3 beta (Ser9)/beta-cateninisurvivin. These results indicated that the potential of Glut1 as a therapeutic target should be carefully reevaluated.
- Files in This Item
-
Go to Link
- Appears in
Collections - 서울 자연과학대학 > 서울 생명과학과 > 1. Journal Articles
![qrcode](https://api.qrserver.com/v1/create-qr-code/?size=55x55&data=https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/18605)
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.