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 Nov 4;12:11271–11283. doi: 10.2147/CMAR.S255895

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

© 2020 Zhu 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

Down-regulation of CDK1 inhibited migration, invasion and promoted apoptosis in fluorouracil-resistant CRC cells.

Notes: (A and B) Wound healing assays were performed to evaluate cellular migration. CDK1 knockdown significantly inhibited the migration ability. (C and D) Transwell assays were performed to evaluate cellular invasion. Silencing of CDK1 attenuated the invasive ability of HT-29/5-Fu and SW480/5-Fu. (E and F) Apoptosis was determined by flow cytometry assays in CRC cells treated with 5-Fu. Inhibition of CDK1 promoted cell apoptosis in CRC cell lines. *P<0.05, **P<0.01, ***P<0.001.