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 Jun 5;12:4461–4468. doi: 10.2147/OTT.S210077

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

© 2019 Wang 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

Vitexin inhibited cell growth by inducing cell apoptosis in nasopharyngeal carcinoma. (A) The chemical structure of vitexin (VTX). (B) Four NPC cell lines were incubated with indicated concentrations of vitexin for 24 hrs, followed by CCK-8 assay. (C) CNE1 and HK1 cells were treated with vehicle (NC) or 10 μM vitexin for 24 hrs, followed by PI staining and analysis on a flow cytometer. (D) CNE1 and HK1 cells were treated with 0, 5, 10 or 20 μM vitexin for 24 hrs, followed by immunoblotting against Cyclin D1, p21 and p53. GAPDH was used as an internal control. (E) CNE1 and HK1 cells were treated with increasing concentrations of vitexin for 24 hrs, followed by immunoblotting against PARP, Bcl-2, Mcl1 and GAPDH.