Research Papers:
Cofilin 1 promotes bladder cancer and is regulated by TCF7L2
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Abstract
Fei Wang1,*, Dinglan Wu2,*, Housheng Fu1, Fengrong He1, Congjie Xu1, Jiaquan Zhou1, Daoyuan Li1, Guoping Li1, Jianbing Xu1, Qinghui Wu1, Jianxiang Chen1, Liangju Su1, Weifu Wang1 and Shufang Zhang3
1Department of Urology, People’s Hospital of Hainan Province, Haikou, China
2The Clinical Innovation & Research Center (CIRC), Shenzhen Hospital, Southern Medical University, Shenzhen, China
3Central 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: [email protected]
Weifu Wang, email: [email protected]
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.
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