ArticleInternational journal of biological sciences2022
High Expression of G6PD Increases Doxorubicin Resistance in Triple Negative Breast Cancer Cells by Maintaining GSH Level.
Article in International journal of biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 49 citations in OpenAlex.
- G6PD: An Old Player with Multiple Emerging Roles from Cancer Progression to Metastasis and Chemoresistance.The protein journal · 2026Review
- Targeting non-coding RNAs in the ferroptosis system: Molecular mechanisms and clinical translation for reversing doxorubicin resistance in breast cancer.Non-coding RNA research · 2026Review
- Disulfidptosis and its molecular mechanisms in cancer: mechanisms, regulation, and therapeutic potential.Medical oncology (Northwood, London, England) · 2026Review
- ICAM2 promotes endocrine resistance via dynein-mediated OXPHOS activation in ER-positive breast cancer.Cell death & disease · 2026Article
- Metabolic Vulnerabilities as a Therapeutic Target in Breast Cancer.Current oncology (Toronto, Ont.) · 2026Review
- Synergistic mechanism of Shengyang Shiyiwei Pill in enhancing bevacizumab efficacy for hepatocellular carcinoma-associated ascites.Annals of medicine and surgery (2012) · 2026Article
- Glucose metabolic reprogramming: a novel strategy to enhance radiotherapy response to triple-negative breast cancer.Frontiers in public health · 2026Review
- Recent advances in nanoparticles-based sonodynamic and immune checkpoint blockade synergistic therapy for pancreatic ductal adenocarcinoma.Materials today. Bio · 2025Review
- Immunometabolism: crosstalk with tumor metabolism and implications for cancer immunotherapy.Molecular cancer · 2025Review
- A review of the pathogenesis of mitochondria in breast cancer and progress of targeting mitochondria for breast cancer treatment.Journal of translational medicine · 2025Review
- The Landscape of Potential Targeted Treatments and Chemotherapy Efficacy Biomarkers for TNBC.Breast cancer (Dove Medical Press) · 2025Review
- Single-cell sequencing and spatial transcriptomics reveal the evolution of glucose metabolism in hepatocellular carcinoma and identify G6PD as a potential therapeutic target.Frontiers in oncology · 2025Article
- Review
- PRKDC Induces Chemoresistance in Osteosarcoma by Recruiting GDE2 to Stabilize GNAS and Activate AKT.Cancer research · 2024Article
- G6PD maintains the VSMC synthetic phenotype and accelerates vascular neointimal hyperplasia by inhibiting the VDAC1-Bax-mediated mitochondrial apoptosis pathway.Cellular & molecular biology letters · 2024Article
- Antiproliferative and Apoptotic Effects of Tempol, Methotrexate, and Their Combinations on the MCF7 Breast Cancer Cell Line.ACS omega · 2024Article
- Reprogramming of glucose metabolism: Metabolic alterations in the progression of osteosarcoma.Journal of bone oncology · 2024Review
- Targeting the initiator to activate both ferroptosis and cuproptosis for breast cancer treatment: progress and possibility for clinical application.Frontiers in pharmacology · 2024Review
- The Emerging Roles of the Metabolic Regulator G6PD in Human Cancers.International journal of molecular sciences · 2023Review
- Ascorbate Uptake and Retention by Breast Cancer Cell Lines and the Intracellular Distribution of Sodium-Dependent Vitamin C Transporter 2.Antioxidants (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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