Ovarian Cancer Relies on Glucose Transporter 1 to Fuel Glycolysis and Growth: Anti-Tumor Activity of BAY-876
Open accessAbstract
The recent progresses in understanding of cancer glycolytic phenotype have offered new strategies to manage ovarian cancer and other malignancies. However, therapeutic targeting of glycolysis to treat cancer remains unsuccessful due to complex mechanisms of tumor glycolysis and the lack of selective, potent and safe glycolytic inhibitors. Recently, BAY-876 was identified as a new-generation inhibitor of glucose transporter 1 (GLUT1), a GLUT isoform commonly overexpressed but functionally poorly defined in ovarian cancer. Notably, BAY-876 has not been evaluated in any cell or preclinical animal models since its discovery. We herein took advantage of BAY-876 and molecular approaches to study GLUT1 regulation, targetability, and functional relevance to cancer glycolysis. The anti-tumor activity of BAY-876 was evaluated with ovarian cancer cell line- and patient-derived xenograft (PDX) models. Our results show that inhibition of GLUT1 is sufficient to block basal and stress-regulated glycolysis, and anchorage-dependent and independent growth of ovarian cancer cells. BAY-876 dramatically inhibits tumorigenicity of both cell line-derived xenografts and PDXs. These studies provide direct evidence that GLUT1 is causally linked to the glycolytic phenotype in ovarian cancer. BAY-876 is a potent blocker of GLUT1 activity, glycolytic metabolism and ovarian cancer growth, holding promise as a novel glycolysis-targeted anti-cancer agent.
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BAY-876, a potent GLUT1 inhibitor, was effective in preclinical settings.
“BAY-876, a potent GLUT1 inhibitor49, was separately shown as an effective candidate in pre-clinical setting 50.”
From The metabolic landscape of RAS-driven cancers from biology to therapy (2021) · cites this paper as [50]
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- Authors
- Ma, Y., Wang, W., Idowu, M. O., Oh, U., Wang, X.-Y., Temkin, S. M., & Fang, X.
- Affiliations
- Virginia Commonwealth University (US)
- Corresponding author
- Fang, Xianjun
- Venue
- Cancers
- Publisher
- MDPI AG
- Published
- 2018-12-31
- Volume
- 11
- Issue
- 1
- Pages
- 33
- ISSN
- 2072-6694 (ISSN-L)
- PMC
- PMC6356953
- OpenAlex
- W2907710771
- Cited by
- 145
- References
- 51
- Citations by year
- 2026: 14 · 2025: 15 · 2024: 21 · 2023: 25 · 2022: 18 · 2021: 27 · 2020: 9 · 2019: 14
- FWCI
- 3.85
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- Cancers (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institutes of Health (P30 CA16059)
- Astar Biotechnology Research award (N/A)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Reproductive Medicine › Ovarian cancer diagnosis and treatment
- Keywords
- ovarian cancer, glucose transporter 1, GLUT1, BAY-876, glycolysis, cancer metabolism, glycolysis inhibitors, tumor growth, patient-derived xenografts, anchorage-independent growth, anticancer activity
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