Please use this identifier to cite or link to this item:
Title: High expression of G6PD increases doxorubicin resistance in triple negative breast cancer cells by maintaining GSH level
Authors: Luo, Man
Fu, Afu
Wu, Renfei
Wei, Na
Song, Kai
Lim, Sierin
Luo, Kathy Qian
Keywords: Engineering::Bioengineering
Issue Date: 2022
Source: Luo, M., Fu, A., Wu, R., Wei, N., Song, K., Lim, S. & Luo, K. Q. (2022). High expression of G6PD increases doxorubicin resistance in triple negative breast cancer cells by maintaining GSH level. International Journal Of Biological Sciences, 18(3), 1120-1133.
Project: MOE2014-T2-1-025 
Journal: International Journal Of Biological Sciences 
Abstract: Resistance to doxorubicin (DOX) remains a big challenge to breast cancer treatment especially for triple negative breast cancer (TNBC). Our previous study revealed that the antioxidant system plays an important role in conferring metastasis derived DOX resistance. In this study, we used two-dimensional difference gel electrophoresis (2D-DIGE) proteomics to compare the expression profiles of two generations of TNBC cell lines which have increased metastatic ability in nude mice and exhibited resistance to DOX. Through careful analyses, one antioxidant protein: glucose-6-phosphate dehydrogenase (G6PD) was identified with 3.2-fold higher level in metastatic/DOX-resistant 231-M1 than its parental 231-C3 cells. Analyses of clinical data showed that TNBC patients with higher G6PD levels exhibited lower overall survival than patients with lower G6PD level. Reducing G6PD expression by siRNA or inhibiting its activity with dehydroepiandrosterone (DHEA) significantly increased DOX's cytotoxicity in both cell lines. Importantly, inhibiting G6PD's activity with DHEA dramatically increased the apoptotic rate of 1.25 µM DOX from 2% to 54%. Our results suggest that high level of G6PD can help TNBC to resist DOX-induced oxidative stress. Thus, inhibiting G6PD shall be a good strategy to treat DOX-resistant TNBC.
ISSN: 1449-2288
DOI: 10.7150/ijbs.65555
Schools: Interdisciplinary Graduate School (IGS) 
School of Chemical and Biomedical Engineering 
Rights: © The author(s). This is an open access article distributed under the terms of the Creative Commons Attribution License ( See for full terms and conditions.
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:IGS Journal Articles
SCBE Journal Articles

Files in This Item:
File Description SizeFormat 
v18p1120.pdf2.81 MBAdobe PDFThumbnail

Citations 20

Updated on Dec 3, 2023

Web of ScienceTM
Citations 20

Updated on Oct 25, 2023

Page view(s)

Updated on Dec 4, 2023


Updated on Dec 4, 2023

Google ScholarTM




Items in DR-NTU are protected by copyright, with all rights reserved, unless otherwise indicated.