AffiliationThe Sidney Kimmel Cancer Center, Thomas Jefferson University, 233 South 10th Street, Philadelphia, Pennsylvania 19107, USA
MetadataShow full item record
AbstractAwareness that the metabolic phenotype of cells within tumours is heterogeneous - and distinct from that of their normal counterparts - is growing. In general, tumour cells metabolize glucose, lactate, pyruvate, hydroxybutyrate, acetate, glutamine, and fatty acids at much higher rates than their nontumour equivalents; however, the metabolic ecology of tumours is complex because they contain multiple metabolic compartments, which are linked by the transfer of these catabolites. This metabolic variability and flexibility enables tumour cells to generate ATP as an energy source, while maintaining the reduction-oxidation (redox) balance and committing resources to biosynthesis - processes that are essential for cell survival, growth, and proliferation. Importantly, experimental evidence indicates that metabolic coupling between cell populations with different, complementary metabolic profiles can induce cancer progression. Thus, targeting the metabolic differences between tumour and normal cells holds promise as a novel anticancer strategy. In this Review, we discuss how cancer cells reprogramme their metabolism and that of other cells within the tumour microenvironment in order to survive and propagate, thus driving disease progression; in particular, we highlight potential metabolic vulnerabilities that might be targeted therapeutically.
CitationCancer metabolism: a therapeutic perspective. 2016: Nat Rev Clin Oncol
JournalNature Reviews. Clinical oncology
- Metabolic coupling and the Reverse Warburg Effect in cancer: Implications for novel biomarker and anticancer agent development.
- Authors: Wilde L, Roche M, Domingo-Vidal M, Tanson K, Philp N, Curry J, Martinez-Outschoorn U
- Issue date: 2017 Jun
- Metabolic and genetic regulation of cardiac energy substrate preference.
- Authors: Kodde IF, van der Stok J, Smolenski RT, de Jong JW
- Issue date: 2007 Jan
- Mitochondrial fission induces glycolytic reprogramming in cancer-associated myofibroblasts, driving stromal lactate production, and early tumor growth.
- Authors: Guido C, Whitaker-Menezes D, Lin Z, Pestell RG, Howell A, Zimmers TA, Casimiro MC, Aquila S, Ando' S, Martinez-Outschoorn UE, Sotgia F, Lisanti MP
- Issue date: 2012 Aug
- The Warburg effect in tumor progression: mitochondrial oxidative metabolism as an anti-metastasis mechanism.
- Authors: Lu J, Tan M, Cai Q
- Issue date: 2015 Jan 28
- Doxorubicin increases oxidative metabolism in HL-1 cardiomyocytes as shown by 13C metabolic flux analysis.
- Authors: Strigun A, Wahrheit J, Niklas J, Heinzle E, Noor F
- Issue date: 2012 Feb