TY - JOUR
T1 - PI3K keeps the balance between metabolism and cancer
AU - Braccini, L.
AU - Ciraolo, E.
AU - Martini, M.
AU - Pirali, T.
AU - Germena, G.
AU - Rolfo, K.
AU - Hirsch, E.
N1 - Funding Information:
This work was supported by grants from AIRC, Fondazione Cariplo-Ricerca Biomedica 2009, Regione Piemonte .
PY - 2012/9
Y1 - 2012/9
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84864554955&partnerID=8YFLogxK
U2 - 10.1016/j.jbior.2012.04.002
DO - 10.1016/j.jbior.2012.04.002
M3 - Review article
SN - 2212-4926
VL - 52
SP - 389
EP - 405
JO - Advances in Biological Regulation
JF - Advances in Biological Regulation
IS - 3
ER -