ArticleNature communications2020
GLUT1 inhibition blocks growth of RB1-positive triple negative breast cancer.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 164 papers.
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Who cites it
164 citing papers in PubMed, 290 citations in OpenAlex.
- Disulfidptosis-based cancer therapy: Opportunity and challenge.Genes & diseases · 2027Review
- Lysyl oxidase inhibition disrupts mitochondrial homeostasis to create vulnerability to ferroptosis in TNBC.Cell reports. Medicine · 2026Article
- Targeting GLUTs in Cancer: Mechanisms, Combination Strategies, and Translational Challenges.Current medical science · 2026Review
- YTHDC1 Orchestrates Glucose and Glutamate Rewiring to Overcome Lethal Metabolic Stress in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Glucose and Glutamine Deprivation Promotes Breast Cancer Lung Metastasis via BRD4-Dependent Enhancer Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- CDCA4 Promotes Lipid Metabolism in Triple-Negative Breast Cancer Through Activation of the SESN2/mTOR/SREBP1 Pathway.Cancers · 2026Article
- Glucose Transporter 1 in Health and Disease.MedComm · 2026Review
- An in vivo platform to jointly monitor cellular and metabolic responses to chemotherapy.bioRxiv : the preprint server for biology · 2026Article
- Solute carrier transporters as metabolic gatekeepers in tumor-microenvironment crosstalk.Acta pharmacologica Sinica · 2026Review
- GLUT6-facilitated noncanonical glucose metabolic rewiring enables resistance to targeted cancer therapy.Nature communications · 2026Article
- Targeted Delivery of GLUT1 Inhibitor via Macrophage Nanovesicles for Pulmonary Arterial Hypertension Therapy.Journal of extracellular vesicles · 2026Article
- Neu5Gc-associated Serum Immunoglobulin G Glycosylation as a Diagnostic Biomarker for Hepatocellular Carcinoma.Journal of clinical and translational hepatology · 2026Article
- Mitochondrial dynamics and cancer: mechanisms and targeted therapy.Cell biology and toxicology · 2026Review
- Nutrient Availability Dictates Cancer Metabolism-Based Therapeutic Responses to Nononcology Drugs.Cancer research · 2026Article
- AMPK-activated BAP1 regulates pVHL stability and tumor-suppressive functions.Cell death and differentiation · 2026Article
- Emerging Protein Targets in Triple-Negative Breast Cancer: Beyond Conventional Therapy.Cancers · 2026Review
- Metabolic reprogramming in cancer: signaling pathways and therapeutic targets.Molecular cancer · 2026Review
- D-glucose uptake inhibits bovine alphaherpesvirus 1 post-binding cell process entry via inhibition of PLC-γ1 signaling in a glucose transporter 1-independent manner.Microbiology spectrum · 2026Article
- SLC2A1Nature cell biology · 2026Article
- RB1-I680T mutation potentiates tumor growth and chemotherapy sensitivity in non-small cell lung cancer via derepressing E2F1 transcription.Cell communication and signaling : CCS · 2026Article
104 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
29 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple negative breast cancer (TNBC) is a deadly form of breast cancer due to the development of resistance to chemotherapy affecting over 30% of patients. New therapeutics and companion biomarkers are urgently needed. Recognizing the elevated expression of glucose transporter 1 (GLUT1, encoded by SLC2A1) and associated metabolic dependencies in TNBC, we investigated the vulnerability of TNBC cell lines and patient-derived samples to GLUT1 inhibition. We report that genetic or pharmacological inhibition of GLUT1 with BAY-876 impairs the growth of a subset of TNBC cells displaying high glycolytic and lower oxidative phosphorylation (OXPHOS) rates. Pathway enrichment analysis of gene expression data suggests that the functionality of the E2F pathway may reflect to some extent OXPHOS activity. Furthermore, the protein levels of retinoblastoma tumor suppressor (RB1) strongly correlate with the degree of sensitivity to GLUT1 inhibition in TNBC, where RB1-negative cells are insensitive to GLUT1 inhibition. Collectively, our results highlight a strong and targetable RB1-GLUT1 metabolic axis in TNBC and warrant clinical evaluation of GLUT1 inhibition in TNBC patients stratified according to RB1 protein expression levels.
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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.