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 Aug 18;7:8803. doi: 10.1038/s41598-017-09169-2

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

© The Author(s) 2017

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/.

PMC Copyright notice

Functional assays revealing that ADAR2 presents oncogenic functions in vitro. HEC-1A, Ishikawa and RL95-2 EC cell lines were used for the functional assays. Panel A. Proliferation assay showing a significant decrease in cell viability (OD 590 nm) in the 3 cell lines when inhibiting ADAR2 expression. Panel B. Apoptosis assay showing a significant increase in apoptosis rate when silencing ADAR2. Panel C. Wound healing assay indicating a significant decrease in HEC-1A and RL95-2 migration capabilities (% of wound healing) when treating cells with siRNA-ADAR2. No significant changes were seen when inhibiting ADAR1.