Glycolysis inhibition for anticancer treatment
By H. Pelicano, D. Martin, R. Xu, Peng Huang. Oncogene, 2006
1,515 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/e423abf57ea9a097a63f3041c31f05613d19f7d6
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
- David B. Graves
- D. Y. Gui
- Alba Luengo
- Ming Tan
- J. Chiche
- G. J. Yoshida
- M. Brahimi-Horn
- M. V. Vander Heiden
In Molecular Biology
- David B. Graves
- D. Y. Gui
- Ming Tan
- Alba Luengo
- J. Chiche
- G. J. Yoshida
- M. Brahimi-Horn
- M. V. Vander Heiden
Citations in the corpus
- Targeting cellular metabolism to improve cancer therapeutics (2013, background): “Accumulation of 2-DG inhibits glycolysis causing ATP depletion, cell cycle inhibition and cell death.(32,33) Under normoxic conditions, 2-DG can interfere with N-linked glycosylation and induce an unfolded protein response, leading to”
- Reprogramming of human primary somatic cells by OCT4 and chemical compounds. (2010, background): “…glycolytic metabolism enhance reprogramming 654 Cell Stem Cell 7, December 3, 2010 ª20 (such as 2,4-dinitrophenol and N-oxaloylglycine), whereas compounds that block glycolytic metabolism inhibit reprogramming (such as oxalate) (Figure 2G) (Hewitson and Schofield, 2004; Pelicano et al., 2006).”
- Tumor glycolysis as a target for cancer therapy: progress and prospects (2013, neutral): “GLUT 1, GLUT 3) [6,7] thus facilitating”
- Tumour hypoxia induces a metabolic shift causing acidosis: a common feature in cancer (2009, background): “This study reinforced the idea that manipulating hypoxic tumour metabolism by targeting specific HIFinduced glycolytic enzymes could participate in bringing about a metabolic deficiency through an indirect block in ATP production [10, 123].”
- Hypoxia and cancer (2007, background): “phenotype may provide tumour-specific agents that hold the advantage of sparing normal tissue [59–61], which is not the case with classical chemotherapy.”
- Distribution and biological activities of the flavonoid luteolin. (2009, background): “The activation of glycolysis is essential for cancer cells to keep ATP levels and to provide building blocks for biosynthesis during cell proliferation [181, 182].”
- Metabolic reprogramming: the emerging concept and associated therapeutic strategies (2015, background): “Tumor cells finely regulate ATP synthesis by regulating substrate uptake, as well as enzymes related to glycolysis, which enables them adapt to the nutrient microenvironment [33].”
- Nanoparticles for Cancer Therapy: Current Progress and Challenges (2021, background): “This is the chief source of energy for cell division [34] and makes the surrounding environment acidic.”
- Nanoparticle-Based Drug Delivery in Cancer Therapy and Its Role in Overcoming Drug Resistance (2020, background): “Unlike nanovaccines, artificial APCs function with MHC-antigen complexes and costimulatory molecules that directly bind to T cell receptors (TCRs) and co-stimulatory receptors on T cells, respectively, resulting in T cell activation (Perica et al., 2014).”
- The emerging role of reactive oxygen and nitrogen species in redox biology and some implications for plasma applications to medicine and biology (2012, background): “Table 2 lists a set of drugs commonly in use today that cause ROS stress either through pro-oxidant action or by blocking antioxidants [135].”