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 Oct 29;13:11031–11044. doi: 10.2147/OTT.S266549

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

© 2020 Cai 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

Apatinib inhibited the β-catenin pathway. Apatinib decreased mRNA and protein levels of endogenous β-catenin target genes in HCT116 and CT26 cells. HCT116 cells were treated with 30 μM apatinib for 24 h, and different expression genes were analyzed by RNA-seq. mRNA levels of β-catenin target genes were analyzed (A) and further confirmed by RT-PCR (B). Data shown represent the mean of three independent RT-PCR reactions, graphed as relative expression level compared to that of DMSO-treated control. (C and D) The effects of apatinib on β-catenin target gene products in HCT116 (C) and CT26 cells (D) were examined through Western blot analyses. The level of β-actin was used as a loading control. Data are expressed as means ± SEM of three experiments. *P < 0.05, **P < 0.01 vs control group.