Open Access Research article

Does phosphorylation of cofilin affect the progression of human bladder cancer?

Hong Chung1, Bokyung Kim2, Seung-Hyo Jung2, Kyung-Jong Won2, Xiaowen Jiang2, Chang-Kwon Lee2, So Dug Lim3, Sang-Kuk Yang1, Ki Hak Song4 and Hong Sup Kim1*

  • * Corresponding author: Hong S Kim hskim@kku.ac.kr

  • † Equal contributors

Author Affiliations

1 Departments of Urology, School of Medicine, Konkuk University, 82 Gugwon-daero, Chungju, Chungbuk, 380-704, Republic of Korea

2 Department of Physiology, School of Medicine, Konkuk University, 82 Gugwon-daero, Chungju, Chungbuk, 380-704, Republic of Korea

3 Department of Pathology, School of Medicine, Konkuk University, Hwayang-dong, Gwanjin-gu, Seoul, 143-792, Republic of Korea

4 Departments of Urology, College of Medicine, Chungnam National University, Chungnam, Republic of Korea

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BMC Cancer 2013, 13:45  doi:10.1186/1471-2407-13-45

Published: 1 February 2013

Abstract

Background

We determined the differently expressed protein profiles and their functions in bladder cancer tissues with the aim of identifying possible target proteins and underlying molecular mechanisms for taking part in their progression.

Methods

We examined the expression of proteins by proteomic analysis and western blot in normal urothelium, non-muscle-invasive bladder cancers (NMIBCs), and muscle-invasive bladder cancers (MIBCs). The function of cofilin was analyzed using T24 human bladder cancer cells.

Results

The expression levels of 12 proteins were altered between bladder cancers and normal bladder tissues. Of these proteins, 14-3-3σ was upregulated in both NMIBCs and MIBCs compared with controls. On the other hand, myosin regulatory light chain 2, galectin-1, lipid-binding AI, annexin V, transthyretin, CARD-inhibitor of NF-κB-activating ligand, and actin prepeptide were downregulated in cancer samples. Cofilin, an actin-depolymerizing factor, was prominent in both NMIBCs and MIBCs compared with normal bladder tissues. Furthermore, we confirmed that cofilin phosphorylation was more prominent in MIBCs than in NMIBCs using immunoblotting and immunohistochemcal analyses. Epidermal growth factor (EGF) increased the phosphorylation of cofilin and elevated the migration in T24 cells. Knockdown of cofilin expression with small interfering RNA attenuated the T24 cell migration in response to EGF.

Conclusions

These results demonstrate that the increased expression and phosphorylation of cofilin might play a role in the occurrence and invasiveness of bladder cancer. We suspected that changes in cofilin expression may participate in the progression of the bladder cancer.

Keywords:
Cofilin; Phosphorylation; Invasion; Urothelial cell carcinoma