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. 2022 Jul 8;13:3955. doi: 10.1038/s41467-022-31645-1

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — AKT is activated in a cascade of events. Upstream stimuli, such as growth factors and cytokines, induce the production of phosphatidylinositol (3,4,5) trisphosphates (PIP3) by phosphoinositide 3-kinase (PI3K). These phospholipids serve as plasma membrane docking sites for AKT and PDK1 at pleckstrin-homology (PH) domains. PDK1 phosphorylates AKT at Thr308 at the plasma membrane which partially activates AKT, whereas AKT is fully activated after phosphorylation at Ser473 by mTORC2. PRMT5 methylates AKT1 on R15 in the PH domain, by which it promotes AKT1 association with the plasma membrane and subsequent phosphorylation by PDK1 and mTORC2. Downstream of AKT signaling, PRMT5 increases the expression of EMT transcription factors, such as SNAIL, ZEB1, and TWIST1 augmenting the EMT program to promote tumor metastasis.