Abstract
Epidemiological studies have established a positive correlation between cancer and metabolic disorders, suggesting that aberrant cell metabolism is a common feature of nearly all tumors. To meet their demand of building block molecules, cancer cells switch to a heavily glucose-dependent metabolism. As insulin triggers glucose uptake, most tumors are or become insulin-dependent. However, the effects of insulin and of other similar growth factors are not only limited to metabolic control but also favor tumor growth by stimulating proliferation and survival. A key signaling event mediating these metabolic and proliferative responses is the activation of the phosphatidylinositol-3 kinases (PI3K) pathway. In this review, we will thus discuss the current concepts of tumor metabolism and the opportunity of PI3K-targeted therapies to exploit the "sweet tooth" of cancer cells.
| Lingua originale | Inglese |
|---|---|
| pagine (da-a) | 389-405 |
| Numero di pagine | 17 |
| Rivista | Advances in Biological Regulation |
| Volume | 52 |
| Numero di pubblicazione | 3 |
| DOI | |
| Stato di pubblicazione | Pubblicato - set 2012 |
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