Cofilin 1 promotes bladder cancer and is regulated by TCF7L2

// Fei Wang 1, * , Dinglan Wu 2, * , Housheng Fu 1 , Fengrong He 1 , Congjie Xu 1 , Jiaquan Zhou 1 , Daoyuan Li 1 , Guoping Li 1 , Jianbing Xu 1 , Qinghui Wu 1 , Jianxiang Chen 1 , Liangju Su 1 , Weifu Wang 1 and Shufang Zhang 3 1 Department of Urology, People’s Hospital of Hainan Province, Haikou, China 2 The Clinical Innovation & Research Center (CIRC), Shenzhen Hospital, Southern Medical University, Shenzhen, China 3 Central Laboratory, Haikou People’s Hospital, Central South University Xiangya School of Medicine Affiliated Haikou Hospital, Haikou, China * These have authors contributed equally to this work Correspondence to: Shufang Zhang, email: haikoushufang@126.com Weifu Wang, email: 13698987211@163.com Keywords: bladder cancer, Cofilin 1, transcription factor 7-like 2 (TCF7L2), depolymerizing factor (ADF), luciferase assay Received: February 02, 2017 Accepted: June 27, 2017 Published: September 06, 2017 ABSTRACT Earlier reports demonstrated that Cofilin expression is increased in bladder cancer samples, though its function remains unknown. Here, we found that Cofilin 1 expression was higher in bladder cancer tissues than in paracancerous tissues. Overexpression of Cofilin 1 promoted, while Cofilin 1 knockdown inhibited, proliferation, migration, and invasion in the T24 and RT4 bladder cancer cell lines. In addition, Cofilin 1 overexpression increased, while Cofilin 1 knockdown decreased, bladder tumor volumes in mouse xenograft experiments. Transcription factor 7-like 2 (TCF7L2) targeted the promoter of the Cofilin 1 gene, and TCF7L2 knockdown or mutations in the Cofilin 1 promoter dramatically decreased Cofilin 1 transcription. TCF7L2 promoted cell proliferation and migration and increased Cofilin 1 protein levels in RT4 and T24 cells. Thus, TCF7L2 contributed to Cofilin 1-induced promotion of bladder cancer development by binding to the Cofilin 1 promoter and increasing its expression.