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. 2018 Oct 1;11(10):4854-4861.
eCollection 2018.

Protein kinase TTK promotes proliferation and migration and mediates epithelial-mesenchymal transition in human bladder cancer cells

Feiran Chen  1 , Peikang Wu  1 , Hailong Hu  1 , Dawei Tian  1 , Ning Jiang  1   2 , Changli Wu  1   3
Affiliations

Protein kinase TTK promotes proliferation and migration and mediates epithelial-mesenchymal transition in human bladder cancer cells

Feiran Chen et al. Int J Clin Exp Pathol. .

Abstract

Aim: To investigate the expression level of TTK in bladder cancer, and its role in the proliferation and migration. To investigate the relationship between TTK and epithelial-mesenchymal transition (EMT).

Patients and methods: We compared the expression level of TTK between human bladder cancer tissues and normal bladder epithelial tissues from 70 patients using immunohistochemistry, qRT-PCR and western blotting. Subsequently, we conducted cell viability and cell migration experiments to investigate the effect of TTK on bladder cancer cells. Furthermore, we used qRT-PCR to detect the biomarkers of EMT to examine the relationship between TTK and EMT.

Results: The expression level of TTK was significantly higher in bladder cancer tissues as compared to the adjacent noncancerous tissues (P < 0.001). The qRT-PCR, immunohistochemistry, and western blotting also showed the same trend. Furthermore, cell viability and cell migration assays showed that TTK promoted proliferation and migration of human bladder cancer cells, and mediated EMT.

Conclusion: This study showed that high expression of TTK can promote proliferation and migration, and might mediate the EMT process in human bladder cancer cells.

Keywords: Bladder cancer; EMT; TTK; migration; proliferation.

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Conflict of interest statement

None.

Figures

Figure 1
Figure 1
A. TTK expression in bladder cancer tissues and adjacent noncancerous tissues (n = 70) was analyzed by qRT-PCR. The expression of TTK was significantly higher in bladder cancer tissues than in adjacent non-cancer tissues (***, P < 0.001). B. TTK marker was assayed in four pairs of bladder cancer and normal tissues by western blotting (C, tumor; N, normal), which showed that TTK was highly expressed in human bladder cancer.
Figure 2
Figure 2
The expression of TTK in normal human bladder urothelium and urothelial carcinoma. (A) and (C) show low expression in normal human urothelium; while (B) and (D) show high expression in human urothelial carcinoma.
Figure 3
Figure 3
A. Western blotting showed that TTK expression was down-regulated in human bladder cancer cell lines (EJ, T24 and 5637) after transfection with TTK-siRNA for 48 h. B. Images of migration of different human bladder cancer cell lines in transwell assay. The number of migrated cells in the histograms represented mean values per field (from three fields, mean ± SD) (***, P = 0.0013).
Figure 4
Figure 4
The effects of TTK on cell proliferation. Bladder cancer cell lines were transfected with NC-siRNA and TTK-siRNA for 24, 48, and 72 h. The cell growth was measured by MTT assay. The y-axis represents cell viability based on measured OD560 values. The x-axis represents time course.
Figure 5
Figure 5
Inhibiting TTK expression in EJ, T24 and 5637 cells decreased the expression of N-cadherin and ZEB1, while the expression of E-cadherin was increased (***, P < 0.001).
See this image and copyright information in PMC

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