Open AccessRole of TEAD4 in colorectal cancer cell proliferation and analysis of its mechanism
Author(s) -
Li Zhen,
Zhang Yunjiao,
Li Shuan,
Zou Tianning,
Li Siyuan
Publication year - 2018
Publication title -
precision radiation oncology
Language(s) - English
Resource type - Journals
ISSN - 2398-7324
DOI - 10.1002/pro6.50
Subject(s) - gene knockdown , sulforhodamine b , viability assay , cell growth , transfection , cancer research , colorectal cancer , cell , blot , biology , downregulation and upregulation , chemistry , cell culture , microbiology and biotechnology , cancer , cytotoxicity , genetics , in vitro , gene
Objective Colorectal cancer is one of the major causes of tumor‐related deaths worldwide. Transcriptional factor TEAD4 is a key factor in the YAP–TAZ signaling pathway. The aim of the present study was to investigate the effect and mechanism of TEAD4 knockdown on colorectal cancer cell proliferation. Methods Transient transfection and a lentivirus system were used to achieve transient or stable TEAD4 knockdown in Caco2 and HT‐29 cells. Western blotting was used to detect transfection efficiency and related protein expression. The sulforhodamine B method and EdU Imaging Kits were used to determine cell viability and DNA synthesis. Results Western blotting showed that knockdown of TEAD4 could increase the expression of the cell cycle protein p27 in Caco2 ( F = 45.78, P < 0.001) and HT‐29 ( F = 40.71, P < 0.001) cells. Sulforhodamine B assays showed that cell viability with TEAD4 knockdown was significantly decreased in Caco2 and HT‐29 cells. Results of EdU assays showed that DNA synthesis was significantly inhibited in Caco2 ( P si#2 = 0.001, P si#3 P < 0.001) and HT‐29 cells ( P si#2 = 0.001, P si#3 = 0.011) with knockdown of TEAD4 . Conclusions The present study showed that TEAD4 plays an important role in cell proliferation in the Caco2 and HT‐29 colorectal cancer cell lines, partially through upregulation of p27 , suggesting that TEAD4 is a potential target and biomarker for the development of novel therapeutics for colorectal cancer.