Molecular and cellular regulation of glucose transporter (GLUT) proteins in cancer
By Maria L. Macheda, S. Rogers, J. Best. Journal of Cellular Physiology, 2005
1,219 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/889a3b68ef8d23768b997cfd95a158a8471ae428
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
- M. V. Vander Heiden
- Ming Tan
- Shanmugasundaram Ganapathy-Kanniappan
- J. Geschwind
- Y. Zhao
- Michael P. Hay
- William R. Wilson
- E. B. Butler
In Molecular Biology
- M. V. Vander Heiden
- J. Rathmell
- Ming Tan
- Shanmugasundaram Ganapathy-Kanniappan
- J. Geschwind
- J. Wofford
- Y. Zhao
- Ellen L. Goode
In Oncology
Citations in the corpus
- Targeting hypoxia in cancer therapy (2011, background): “Elevated GLUT1 levels has been described in a wide range of tumour types and has been demonstrated to be a negative prognostic indicato”
- Targeting cellular metabolism to improve cancer therapeutics (2013, background): “The GLUT family of proteins is responsible for this, and are often found dysregulated or overexpressed in malignant cells.(26) The human GLUT family consists of 14 members (GLUT1-14 or SLC2A1-14).”
- Obesity and Diabetes: The Increased Risk of Cancer and Cancer-Related Mortality. (2015, background): “Cells transformed by oncogenes, such as ras, src, and c-myc have been shown to activate GLUT1 and GLUT3 expression (40, 125).”
- Targeting cancer metabolism: a therapeutic window opens (2011, background): “Glucose transporter 1 (GLUT1; also known as SLC2A1) is the glucose transporter with the largest tissue distribution and is thought to be responsible for basal glucose uptake in most cancer cells and normal cell”
- p53 regulates glucose metabolism through an IKK-NF-κB pathway and inhibits cell transformation (2008, background): “The expression of GLUT1 and GLUT3 appears to contribute to glycolysis in several human cancer cell line”
- Common Genetic Variation In Cellular Transport Genes and Epithelial Ovarian Cancer (EOC) Risk (2015, background): “Aberrant expression of transmembrane transport genes has been associated with increased risk, as well as aggressiveness, of a number of cancers including breast [4–7], prostate [8], liver [9], colorectal and colon [10–12], thyroid [13] and neuroblastoma [14].”
- Hexokinase II: Cancer's double-edged sword acting as both facilitator and gatekeeper of malignancy when bound to mitochondria (2006, background): “In human tumors, a high level of Glut-1 expression has been associated with poor prognosis (Macheda et al., 2005).”
- Cytokine stimulation promotes glucose uptake via phosphatidylinositol-3 kinase/Akt regulation of Glut1 activity and trafficking. (2007, background): “Conversely, increased glucose uptake occurs in immune cell activation and in poor prognosis cancers and is required for increased cellular proliferation (Gatenby and Gillies, 2004; Macheda et al., 2005).”
- Tumor glycolysis as a target for cancer therapy: progress and prospects (2013, background): “Phloretin, WZB117, Fasentin) demonstrated anticancer effects in preclinical models [6,85].”
- Hypoxia-Inducible Factors Regulate Tumorigenic Capacity of Glioma Stem Cells (2009, neutral): “The glucose transporter Glut1 is frequently upregulated in cancer cells to facilitate their accelerated metabolism (Macheda et al., 2005; Younes et al., 1995).”