Abstract
BackgroundWe 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.MethodsWe 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.ResultsThe 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.ConclusionsThese 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.
Highlights
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
Myosin regulatory light chain 2, galectin-1, lipid-binding AI, annexin V, transthyretin, CARDinhibitor of NF-κB-activating ligand, actin prepeptide, and macrophage-capping protein were downregulated in bladder tissues from non-muscle-invasive bladder cancers (NMIBCs) and muscle-invasive bladder cancers (MIBCs) samples compared with controls (Figure 2)
In proteomics analysis, we found that the expression of cofilin was significantly increased in bladder cancers without difference between NMIBC and MIBC samples
Summary
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. Bladder cancer is the ninth most often diagnosed and the seventh most prevalent cancer worldwide, and shows an increasing tendency in Asia [1] It commonly presents as an urothelial cell carcinoma with non-muscle-invasive bladder cancer (NMIBC), but is clinically well controlled and can be treated relatively by transurethral resection of bladder tumor. There are several known markers used clinically for bladder cancer: nuclear matrix protein 22, telomerase, epidermal growth factor (EGF) receptor and others [4,5,6,7,8]. These have limitations in their specificity and/or sensitivity, as is shown by cystoscopy of bladder cancers [4]. Celis’ group has performed proteomic and genomic analyses to identify markers in bladder cancers [9,10,11,12]
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