Molecular and cellular regulation of glucose transporter (GLUT) proteins in cancer
Open accessAbstract
Malignant cells are known to have accelerated metabolism, high glucose requirements, and increased glucose uptake. Transport of glucose across the plasma membrane of mammalian cells is the first rate‐limiting step for glucose metabolism and is mediated by facilitative glucose transporter (GLUT) proteins. Increased glucose transport in malignant cells has been associated with increased and deregulated expression of glucose transporter proteins, with overexpression of GLUT1 and/or GLUT3 a characteristic feature. Oncogenic transformation of cultured mammalian cells causes a rapid increase of glucose transport and GLUT1 expression via interaction with GLUT1 promoter enhancer elements. In human studies, high levels of GLUT1 expression in tumors have been associated with poor survival. Studies indicate that glucose transport in breast cancer is not fully explained by GLUT1 or GLUT3 expression, suggesting involvement of another glucose transporter. Recently, a novel glucose transporter protein, GLUT12, has been found in breast and prostate cancers. In human breast and prostate tumors and cultured cells, GLUT12 is located intracellularly and at the cell surface. Trafficking of GLUT12 to the plasma membrane could therefore contribute to glucose uptake. Several factors have been implicated in the regulation of glucose transporter expression in breast cancer. Hypoxia can increase GLUT1 levels and glucose uptake. Estradiol and epidermal growth factor, both of which can play a role in breast cancer cell growth, increase glucose consumption. Estradiol and epidermal growth factor also increase GLUT12 protein levels in cultured breast cancer cells. Targeting GLUT12 could provide novel methods for detection and treatment of breast and prostate cancer. © 2004 Wiley‐Liss, Inc.
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In malignant tumors, transportation and metabolism of glucose lack controls because of the autonomous nature of malignancies, so hyperglycemia would not have a significant effect on tumors.
“However, in malignant tumors transportation and metabolism of glucose lack such controls because of the autonomous nature of malignancies [27,84].Thus, hyperglycemia may lead to competition between endogenous glucose and FDG in normal cells but would not have significant effect on tumors.”
From Effect of blood glucose level on standardized uptake value (SUV) in 18F-FDG PET-scan: a systematic review and meta-analysis of 20,807 individual SUV measurements (2019) · cites this paper as [27]
The Abstract (page not available) reports increased glucose uptake and deregulated GLUT expression in malignant cells, supporting part of the premise. But the paper also describes regulation of tumor glucose uptake by hypoxia and other factors; its “Glucose uptake in tumors” section does not establish that hyperglycemia has no significant effect on tumors or their FDG uptake. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThe prominent type of muscle glucose transporter is GLUT4, which is insulin-dependent, in contrast to tumors, which mainly overexpress Glut-1 and Glut-3 transporters that are not insulin-sensitive.
“The prominent type of muscle glucose transporter is GLUT4, which is insulin-dependent [30,31,93], in contrast to tumors which mainly overexpress Glut-1 and Glut-3 transporters, which are not insulin-sensitive [27,29,94].”
From Effect of blood glucose level on standardized uptake value (SUV) in 18F-FDG PET-scan: a systematic review and meta-analysis of 20,807 individual SUV measurements (2019) · cites this paper as [27]
The Abstract says GLUT4 moves to the muscle-cell membrane in response to insulin and describes GLUT1 and/or GLUT3 overexpression as characteristic of malignant cells. It does not establish that GLUT4 is the predominant muscle transporter or explicitly state that both GLUT1 and GLUT3 are insulin-insensitive. (LLM, conf=0.83)
Experimental — accuracy not yet measured
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- Authors
- Macheda, M. L., Rogers, S., & Best, J. D.
- Affiliations
- The University of Melbourne (AU)
- Corresponding author
- Best, James D.
- Venue
- Journal of Cellular Physiology
- Publisher
- Wiley
- Published
- 2004-08-17
- Volume
- 202
- Issue
- 3
- Pages
- 654-662
- ISSN
- 0021-9541 (ISSN-L)
- 1097-4652
- OpenAlex
- W1971859682
- Cited by
- 1,229
- References
- 120
- Citations by year
- 2026: 24 · 2025: 50 · 2024: 45 · 2023: 64 · 2022: 74 · 2021: 88 · 2020: 78 · 2019: 58 · 2018: 76 · 2017: 72 · 2016: 82 · 2015: 72 · 2014: 69 · 2013: 69 · 2012: 66
- FWCI
- 1.21
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Cellular Physiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Medical Research Council
- National Health and Medical Research Council
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- glucose transporters, GLUT1, GLUT3, GLUT12, cancer metabolism, glucose uptake, breast cancer, prostate cancer, hypoxia, estradiol, epidermal growth factor
- MeSH terms
- Animals, Hypoxia, Glucose, Growth Substances, Hormones, Humans, Monosaccharide Transport Proteins, Neoplasms, Protein Conformation, Gene Expression Regulation, Neoplastic, Cell Line, Tumor
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