| Literature DB >> 27819060 |
Narendra Thapa1, Xiaojun Tan2, Suyong Choi1, Paul F Lambert3, Alan C Rapraeger4, Richard A Anderson5.
Abstract
Phosphoinositide 3-kinase (PI3K) generation of PI(3,4,5)P3 from PI(4,5)P2 and the subsequent activation of Akt and its downstream signaling cascades (e.g. mTORC1) dominates the landscape of phosphoinositide signaling axis in cancer research. However, PI(4,5)P2 is breaking its boundary as merely a substrate for PI3K and phospholipase C (PLC), and is now an established lipid messenger pivotal for different cellular events in cancer. Here, we review the phosphoinositide signaling axis in cancer, giving due weight to PI(4,5)P2 and its generating enzymes, the phosphatidylinositol phosphate (PIP) kinases (PIPKs). We highlighted how PI(4,5)P2 and PIP kinases serve as a proximal node in phosphoinositide signaling axis and how its interaction with cytoskeletal proteins regulates migratory and invasive nexus of metastasizing tumor cells.Entities:
Keywords: Akt; PI(3,4,5)P3; PI(4,5)P2; PI3K; PIPKIγ
Mesh:
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Year: 2016 PMID: 27819060 PMCID: PMC5094282 DOI: 10.1016/j.trecan.2016.05.009
Source DB: PubMed Journal: Trends Cancer ISSN: 2405-8025