ArticleMolecular oncology2019
SGLT1 is required for the survival of triple-negative breast cancer cells via potentiation of EGFR activity.
Article in Molecular oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Sotagliflozin, a Dual SGLT1/2 Inhibitor, Modulates DNMT1 and Class I/II HDAC Expression in Association With Anticancer Effects in Breast and Lung Cancer Cells.Cell biology international · 2026Article
- Solute Carrier transporters in tumor metabolism and immune modulation: implications for therapy.Journal of translational medicine · 2026Review
- Glucose metabolic reprogramming: a novel strategy to enhance radiotherapy response to triple-negative breast cancer.Frontiers in public health · 2026Review
- Landscape of metabolic alterations and treatment strategies in breast cancer.Genes & diseases · 2025Review
- Envisioning Glucose Transporters (GLUTs and SGLTs) as Novel Intervention against Cancer: Drug Discovery Perspective and Targeting Approach.Current drug targets · 2025Review
- Molecular mechanisms and computational insights into human SGLTs: advancing toward selective SGLT1 inhibition.Frontiers in molecular biosciences · 2025Review
- Breast cancer therapy: from the perspective of glucose metabolism and glycosylation.Molecular biology reports · 2024Review
- Review
- Integrated network pharmacology and cellular assay reveal the biological mechanisms of Limonium sinense (Girard) Kuntze against Breast cancer.BMC complementary medicine and therapies · 2023Article
- SGLT1 as an adverse prognostic factor in invasive ductal carcinoma of the breast.Breast cancer research and treatment · 2023Article
- Circ_0003028 enhances the proliferation and glycolytic capacity and suppresses apoptosis in non-small cell lung cancer cells via the miR-1305/miR-1322-SLC5A1 axis.Annals of translational medicine · 2023Article
- Review
- Potential Therapies Targeting the Metabolic Reprogramming of Diabetes-Associated Breast Cancer.Journal of personalized medicine · 2023Review
- CRISPR/Cas9 application in cancer therapy: a pioneering genome editing tool.Cellular & molecular biology letters · 2022Review
- Integrated analysis reveals effects of bioactive ingredients fromFrontiers in plant science · 2022Article
- Emergence of SGLT2 Inhibitors as Powerful Antioxidants in Human Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- Downregulation of GLUT3 impairs STYK1/NOK-mediated metabolic reprogramming and proliferation in NIH-3T3 cells.Oncology letters · 2021Article
- Metabolism and immunity in breast cancer.Frontiers of medicine · 2021Review
- LncRNA TINCR favors tumorigenesis via STAT3-TINCR-EGFR-feedback loop by recruiting DNMT1 and acting as a competing endogenous RNA in human breast cancer.Cell death & disease · 2021Article
- WDHD1 is essential for the survival of PTEN-inactive triple-negative breast cancer.Cell death & disease · 2020Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Sodium/glucose cotransporter 1 (SGLT1), an essential active glucose transport protein that helps maintain high intracellular glucose levels, was previously shown to interact with epidermal growth factor receptor (EGFR); the SGLT1-EGFR interaction maintains intracellular glucose levels to promote survival of cancer cells. Here, we explore the role of SGLT1 in triple-negative breast cancer (TNBC), which is the most aggressive type of breast cancer. We performed TCGA analysis coupled to in vitro experiments in TNBC cell lines as well as in vivo xenografts established in the mammary fat pad of female nude mice. Tissue microarrays of TNBC patients with information of clinical-pathological parameters were also used to investigate the expression and function of SGLT1 in TNBC. We show that high levels of SGLT1 are associated with greater tumour size in TNBC. Knockdown of SGLT1 compromises cell growth in vitro and in vivo. We further demonstrate that SGLT1 depletion results in decreased levels of phospho-EGFR, and as a result, the activity of downstream signalling pathways (such as AKT and ERK) is inhibited. Hence, targeting SGLT1 itself or the EGFR-SGLT1 interaction may provide novel therapeutics against TNBC.
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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.