Abstract
During tumorigenesis, the shift from oxidative phosphorylation to glycolysis in ATP production accounts for the dramatic change in the cellular metabolism and represents one of the major steps leading to tumour formation. The so-called Warburg effect is currently considered something more than a mere modification in the cellular metabolism. The paradox that during cancer cell proliferation the increase in energy need is supplied by glycolysis can be only explained by taking into account the many roles that intermediates of glycolysis or TCA cycle play in cellular physiology, besides energy production. Recent studies have shown that metabolic intermediates induce changes in chromatin structure or drive neo-angiogenesis. In this review, we present some of the latest findings in the study of cancer metabolism with particular attention to how tumour metabolism and its microenvironment can favour tumour growth and aggressiveness, by hijacking and dampening the anti-tumoral immune response.
| Original language | English |
|---|---|
| Pages (from-to) | 46692-46706 |
| Number of pages | 15 |
| Journal | Oncotarget |
| Volume | 7 |
| Issue number | 29 |
| DOIs | |
| Publication status | Published - 2016 |
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Keywords
- Cancer
- Immune response
- Lymphocytes
- Metabolism
ASJC Scopus subject areas
- Oncology
Cite this
Changing perspective on oncometabolites : From metabolic signature of cancer to tumorigenic and immunosuppressive agents. / Corrado, Mauro; Scorrano, Luca; Campello, Silvia.
In: Oncotarget, Vol. 7, No. 29, 2016, p. 46692-46706.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Changing perspective on oncometabolites
T2 - From metabolic signature of cancer to tumorigenic and immunosuppressive agents
AU - Corrado, Mauro
AU - Scorrano, Luca
AU - Campello, Silvia
PY - 2016
Y1 - 2016
N2 - During tumorigenesis, the shift from oxidative phosphorylation to glycolysis in ATP production accounts for the dramatic change in the cellular metabolism and represents one of the major steps leading to tumour formation. The so-called Warburg effect is currently considered something more than a mere modification in the cellular metabolism. The paradox that during cancer cell proliferation the increase in energy need is supplied by glycolysis can be only explained by taking into account the many roles that intermediates of glycolysis or TCA cycle play in cellular physiology, besides energy production. Recent studies have shown that metabolic intermediates induce changes in chromatin structure or drive neo-angiogenesis. In this review, we present some of the latest findings in the study of cancer metabolism with particular attention to how tumour metabolism and its microenvironment can favour tumour growth and aggressiveness, by hijacking and dampening the anti-tumoral immune response.
AB - During tumorigenesis, the shift from oxidative phosphorylation to glycolysis in ATP production accounts for the dramatic change in the cellular metabolism and represents one of the major steps leading to tumour formation. The so-called Warburg effect is currently considered something more than a mere modification in the cellular metabolism. The paradox that during cancer cell proliferation the increase in energy need is supplied by glycolysis can be only explained by taking into account the many roles that intermediates of glycolysis or TCA cycle play in cellular physiology, besides energy production. Recent studies have shown that metabolic intermediates induce changes in chromatin structure or drive neo-angiogenesis. In this review, we present some of the latest findings in the study of cancer metabolism with particular attention to how tumour metabolism and its microenvironment can favour tumour growth and aggressiveness, by hijacking and dampening the anti-tumoral immune response.
KW - Cancer
KW - Immune response
KW - Lymphocytes
KW - Metabolism
UR - http://www.scopus.com/inward/record.url?scp=84979944251&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84979944251&partnerID=8YFLogxK
U2 - 10.18632/oncotarget.8727
DO - 10.18632/oncotarget.8727
M3 - Review article
AN - SCOPUS:84979944251
VL - 7
SP - 46692
EP - 46706
JO - Oncotarget
JF - Oncotarget
SN - 1949-2553
IS - 29
ER -