Abstract
PI3K is an important node regulating the signaling of several essential biological processes. PI3K catalyzes the phosphorylation in position 3 of the inositol ring of phosphatidyl-inositide producing important lipid second messengers. The products of PI3K activity recruit PDK1 and AKT Ser/Thr kinases to the plasma membrane where they get activated transducing a potent proliferative and anti-apoptotic signal to the cell. PI3K is activated by growth factors, insulin and GPCR activation. Furthermore, PI3K can be activated by direct binding to oncogenic Ras proteins. PI3K is commonly altered in human cancers by point activating mutations or by amplification. Furthermore, other proteins of the route are also altered in human tumors (such as phosphatase and tensin homolog in chromosome 10 or human EGF receptor 2) providing constitutive activation of PI3K. The evidence indicates that the PI3K pathway is a potential target for cancer chemotherapy. Indeed, many companies and academic laboratories have initiated a variety of approaches to inhibit the PI3K pathway at different points. In this work, we review the targeting of PI3K protein for therapeutical intervention.
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