Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Aug 7;10:1152. doi: 10.3389/fonc.2020.01152

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2020 Romero-Garcia, Prado-Garcia and Carlos-Reyes.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

DNA methylation regulates the PI3K/PTEN/AKT/mTOR signaling pathway in the resistance to therapy in cancer. (Left) PI3K induces the phosphorylation and activation of AKT/mTOR. This transduction signal begins with the activation of the membrane tyrosine kinase receptors (RTKs) or G-protein-coupled receptors, which promotes the change of phosphatidylinositol (4,5)-bisphosphate (PIP2) in phosphatidylinositol (3-5)-trisphosphate (PIP3). The activation of PI3K (phosphoinositide-3-kinase) is regulated by the phosphatase and tensin homolog (PTEN) by dephosphorylating PIP3 into PIP2. (Right) We show the aberrant methylation of the PTEN, Spalt-like transcription factor 2 (SALL2), transforming growth factor beta-induced protein (TGFB1), and Lysine (K)-specific demethylase 5A (KDM5A) genes through the high expression of methyltransferase (DNMT3B), s-adenosylmethionine (SAM), H3K27me3, H3K9me2, and H3K4me3, promoting a continued activation of the PI3K/AKT/mTOR signaling pathway associated with resistance therapy in solid tumors. , phosphorylation; ↑, increase; ↓, decrease; , methylation, , radiotherapy.

Inline graphic — DNA methylation regulates the PI3K/PTEN/AKT/mTOR signaling pathway in the resistance to therapy in cancer. (Left) PI3K induces the phosphorylation and activation of AKT/mTOR. This transduction signal begins with the activation of the membrane tyrosine kinase receptors (RTKs) or G-protein-coupled receptors, which promotes the change of phosphatidylinositol (4,5)-bisphosphate (PIP2) in phosphatidylinositol (3-5)-trisphosphate (PIP3). The activation of PI3K (phosphoinositide-3-kinase) is regulated by the phosphatase and tensin homolog (PTEN) by dephosphorylating PIP3 into PIP2. (Right) We show the aberrant methylation of the PTEN, Spalt-like transcription factor 2 (SALL2), transforming growth factor beta-induced protein (TGFB1), and Lysine (K)-specific demethylase 5A (KDM5A) genes through the high expression of methyltransferase (DNMT3B), s-adenosylmethionine (SAM), H3K27me3, H3K9me2, and H3K4me3, promoting a continued activation of the PI3K/AKT/mTOR signaling pathway associated with resistance therapy in solid tumors. , phosphorylation; ↑, increase; ↓, decrease; , methylation, , radiotherapy.