Author:
Cai Fangzhen,Li Jianwei,Zhang Yanmei,Huang Sihuai,Liu Wenbin,Zhuo Weifeng,Qiu Chengzhi
Abstract
Abstract
Background
Targeted drugs are the main methods of RCC treatment. However, drug resistance is common in RCC patients, in-depth study of the drug-resistant mechanism is essential.
Methods
We constructed sunitinib resistant and Twist overexpressed A498 cells, and studied its mechanisms in vitro and in vivo.
Results
In cell research, we found that either sunitinib resistance or Twist overexpression can activate Wnt/β-catenin and EMT signaling pathway, and the sunitinib resistance may work through β-catenin/TWIST/TCF4 trimer. In zebrafish research, we confirmed the similarity of Twist overexpression and sunitinib resistance, and the promoting effect of Twist overexpression on drug resistance.
Conclusions
Sunitinib resistance and Twist overexpression can activate Wnt/β-catenin signaling pathway and EMT to promote the growth and metastasis of RCC cells.
Funder
Natural Science Foundation of Fujian Province
National Key Clinical Specialty Discipline Construction Program of China
Publisher
Springer Science and Business Media LLC
Subject
Cancer Research,Genetics,Oncology