ArticleThe FEBS journal2023
Targeting glucose-6-phosphate dehydrogenase by 6-AN induces ROS-mediated autophagic cell death in breast cancer.
Article in The FEBS journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- G6PD: An Old Player with Multiple Emerging Roles from Cancer Progression to Metastasis and Chemoresistance.The protein journal · 2026Review
- Metabolic drivers of genome instability in cancer: mechanisms and therapeutic opportunities.Experimental hematology & oncology · 2026Review
- Metabolic Vulnerabilities as a Therapeutic Target in Breast Cancer.Current oncology (Toronto, Ont.) · 2026Review
- Glucose metabolic reprogramming: a novel strategy to enhance radiotherapy response to triple-negative breast cancer.Frontiers in public health · 2026Review
- NADPH-Related Enzymes and Cancer: Facts and Insights Into the Application of Immunohistochemistry.Biochemistry research international · 2026Review
- The research progress on the role of glucose-6-phosphate dehydrogenase in immune regulation.PeerJ · 2026Review
- Evaluation of Anticancer Potential ofAntioxidants (Basel, Switzerland) · 2025Article
- Implantation of engineered adipocytes suppresses tumor progression in cancer models.Nature biotechnology · 2025Article
- 6-Aminonicotinamide enhances the efficacy of 5-aminolevulinic acid-mediated photodynamic therapy for neuroblastoma.BMC cancer · 2025Article
- Glycolytic Reprogramming in Uterine Fibroids: Genetic, Transcriptomic, Proteomic, and Metabolomic Insights.Genes · 2025Review
- Somatic CRISPR tumorigenesis and multiomic analysis reveal a pentose phosphate pathway disruption vulnerability in MPNSTs.Science advances · 2025Article
- Spatiotemporal Heterogeneity of Tumor Glucose Metabolism Reprogramming: From Single-Cell Mechanisms to Precision Interventions.International journal of molecular sciences · 2025Review
- Review
- Glucose-6-phosphate dehydrogenase regulates mitophagy by maintaining PINK1 stability.Life metabolism · 2025Article
- Exploring Carbon Dot Nanoparticles for Imaging and Cellular Interaction in Triple-Negative Breast Cancer.International journal of nanomedicine · 2025Article
- 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
- The Role of Glucose-6-Phosphate Dehydrogenase in Skin Cancer Metabolism: A Paradigm Shift in Treatment Approaches.Cancers · 2024Review
- Alterations of urine microRNA-7977/G6PD level in patients with diabetic kidney disease and its association with dysfunction of albumin-induced autophagy in proximal epithelial tubular cells.American journal of physiology. Endocrinology and metabolism · 2024Article
- Article
- Glucose metabolism in B cell malignancies: a focus on glycolysis branching pathways.Molecular oncology · 2024Review
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulation of G6PD involved in the pentose phosphate pathway (PPP) is known to promote tumorigenesis. The PPP plays a pivotal role in meeting the anabolic demands of cancer cells. However, the detailed underlying molecular mechanisms of targeting the G6PD-regulated PPP in breast cancer remain unclear. In this study, we aimed to elucidate the molecular pathways mediating the effects of G6PD on cancer progression. Clinical sample analysis found that the expression of G6PD in breast cancer patients was higher than that in normal controls, and patients with higher G6PD expression had poor survival. Gene knockdown or inhibition of G6PD by 6-AN in MCF-7 and MDA-MB-231 cells significantly decreased cell viability, migration, and colony formation ability. G6PD enzyme activity was inhibited by 6-AN treatment, which caused a transient upregulation of ROS. The elevated ROS was independent of cell apoptosis and thus associated with abnormal activated autophagy. Accumulated ROS levels induced autophagic cell death in breast cancer. Inhibition of G6PD suppresses tumour growth in preclinical models of breast cancer. Our results indicate that targeting the G6PD-regulated PPP could restrain tumours in vitro and in vivo, inhibiting G6PD caused cell death by over-activating autophagy, therefore leading to inhibited proliferation and tumour formation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.