Review
doi: 10.3892/mmr.2019.10121.
Epub 2019 Apr 3.
Research progress on the PI3K/AKT signaling pathway in gynecological cancer (Review)
Affiliations
- PMID: 30942405
- PMCID: PMC6522820
- DOI: 10.3892/mmr.2019.10121
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Review
Research progress on the PI3K/AKT signaling pathway in gynecological cancer (Review)
Mol Med Rep.
2019 Jun.
Abstract
The phosphatidylinositol 3‑kinase (PI3K)/protein kinase B (AKT) signaling pathway is involved in the regulation of multiple cellular physiological processes by activating downstream corresponding effector molecules, which serve an important role in the cell cycle, growth and proliferation. This is a common phenomenon; overactivation of the pathway is present in human malignancies and has been implicated in cancer progression, hence one of the important approaches to the treatment of tumors is rational drug design using molecular targets in the PI3K/AKT signaling pathway. In brief, the present review analyzed the effects of the PI3K/AKT signaling pathway on certain gynecological cancer types.
Figures
Schematic of the PI3K/AKT signaling pathway. RTK recruits PI3K following activation and phosphorylation, and phosphorylates PtdIns (4,5) P2 to PtdIns (–5) P3, which activates AKT by recruiting PDK1 to the PH domain of AKT, thereby activating the entire pathway and regulating cell growth. PI3K, phosphatidylinositol 3-kinase; AKT, protein kinase B; RTK, receptor tyrosine kinase; PtdIns, phosphatidylinositol; PDK1, 3-phosphoinositol-dependent protein kinase-1; PH, plekstrin homology; PTEN, phosphatase and tensin homolog; PDGF, platelet derived growth factor; IGF, insulin-like growth factor; EGF, epidermal growth factor.
Effect of the PI3K/AKT signaling pathway on gynecological tumors. By inactivating PTEN, LKB1 and other regulatory factors, the phosphorylation levels of associated molecules in the PI3K/AKT pathway are altered, and the activity of downstream mTOR is further changed, thereby triggering the occurrence of gynecological cancer. PI3K, phosphatidylinositol 3-kinase; AKT, protein kinase B; RTK, receptor tyrosine kinase; PtdIns, phosphatidylinositol; PDK1, 3-phosphoinositol-dependent protein kinase-1; PH, plekstrin homology; PTEN, phosphatase and tensin homolog; LKB1, serine/threonine kinase 11; TSC2, TSC complex subunit 2; mTOR, mechanistic target of rapamycin kinase; mTORC, mTOR complex 2.
