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

. 2019 Nov 7;12:9395–9405. doi: 10.2147/OTT.S205017

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

© 2019 Zhang et al.

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).

PMC Copyright notice

DNA-PKcs promoted EMT and invasion partly via TGF-β1/Smad signaling. (A and B) The numbers of cells invading through a Transwell membrane and migrating into a scratch wound were significantly increased after TGF-β1 stimulation and reduced following LY2109761 inhibition. In addition, blocking the Smad3 pathway and downregulating DNA-PKcs caused a significant decrease in cell migration and invasion in SCL-1 cells. (C–H) TGF-β1 treatment activated p-Smad2/3 signaling in SCL-1 cells. In addition, the knockdown of DNA-PKcs decreased the p-Smad3 levels. LY2109761 could repress p-Smad3 expression and restore the E-cadherin levels, while mesenchymal markers Vimentin and Slug were decreased. *p<0.05, **p<0.01 vs the NC group. #p<0.05, vs the group transfected with si-Ctrl.