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

. 2017 Jul 3;36(43):5995–6005. doi: 10.1038/onc.2017.202

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

Copyright © 2017 The Author(s)

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/

PMC Copyright notice

Model of Rho/F-actin pathway repression by EWS-FLI1 via MRTFB/YAP-1/TEAD transcriptional perturbation. A673/TR/shEF: left: EWS-FLI1-low state: EWS-FLI1 binds to distal genomic elements of EWS-FLI1-anticorrelated target genes and thereby likely hinders MRTFB/YAP-1/TEAD interaction and transcriptional activation of genes involved in actin–cytoskeletal structure (TAGLN, TPM-1 and CALD-1) or are involved in binding to the extracellular matrix (ECM) and insulin growth factors (IGF; CYR61, CTGF). Low expression of these genes might affect cytoskeletal integrity due to compromised actin polymerization and upstream signalling via ECM–receptor interactions. As a consequence, cells exhibit few focal adhesions and stress fibres (F-actin filaments) and F-actin polymerization is reduced.^{9, 10} Right: upon knockdown of EWS-FLI1 (EWS-FLI1-low), expression of MRTFB/YAP-1/TEAD target genes, which regulate cytoskeletal key factors, is increased and thereby likely promoting signalling via Rho both upstream and downstream of actin polymerization. Consequently, cell morphology is drastically altered with increased numbers of focal adhesions and stress fibres as compared to the high EWS-FLI1 cell state.