PI3K/PDK1/Akt Pathways in Cancer

Phosphoinositide 3-kinases (PI3Ks) enzymes are important signalling molecules involved in a variety of different cellular functions. They use phosphoinositides as substrates and they exert their function through phosphorylation of the D3 position within the inositol ring, generating PtdIns3P, PtdIns(3,4)P2 and PtdIns(3,4,5)P3. The PI3K family contains eight mammalian isoforms grouped into three classes in accordance with substrate specificity and structure. Interestingly, there is a variety of genetic abnormalities observed in the PI3K pathway in cancer, such as activating and deactivating mutations and post-transcriptional epigenetic irregularities. It is a common phenomenon in solid tumours to witness aberrant PI3Kα activity, directly or indirectly resulting from mutations of the respective gene; therefore PI3Kα inhibition is an emerging approach for treating these types of tumours and indeed there are a number of relevant ongoing trials. Nevertheless, emerging evidence supports the role of other PI3K isoforms in cancer as well as the complexity and specificity of activation of PI3K downstream effectors. Indeed, novel signaling pathways and cell functions are continuously identified as regulated by PI3K isoforms in cancer. The combined data indicate that the biological functions of PI3K isoforms are far more complex than presently known and that the overall responses to PI3K-inhibiting drugs are likely to be context-dependent. This Special Issue will cover the recent progress in all areas related to PI3K signaling and cancer.

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