J Cancer 2017; 8(10):1892-1899. doi:10.7150/jca.17638

Research Paper

TBK1 Promote Bladder Cancer Cell Proliferation and Migration via Akt Signaling

Wei Chen*1, Kewang Luo*1, Zhiyi ke1, Bin Kuai2, Shiyang He, Wei Jiang1, Weiren Huang✉1, Zhiming Cai✉1

1. Key Laboratory of Medical Reprogramming Technology, Shenzhen Second People's Hospital, First Affiliated Hospital of Shenzhen University, Shenzhen 518039, China.
2. HYK High-throughput Biotechnology Institute, Shenzhen 518060, China
* These authors contributed equally to this work.

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Chen W, Luo K, ke Z, Kuai B, He S, Jiang W, Huang W, Cai Z. TBK1 Promote Bladder Cancer Cell Proliferation and Migration via Akt Signaling. J Cancer 2017; 8(10):1892-1899. doi:10.7150/jca.17638. Available from http://www.jcancer.org/v08p1892.htm

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Bladder cancer is a challenging and fatal malignancy and the improvement in prognosis is limited over years. Deep understanding the mechanism of bladder cancer tumorigenesis and progression will help to discover novel and effective treatment strategies. In this study, we identify non-canonical IkB kinase TBK1 is up-regulated in bladder cancer tissue and cell lines. Knockdown of TBK1 markedly inhibits cell proliferation and migration. Inhibition of TBK1 kinase activity by BX795 significantly attenuates bladder cancer cell proliferation and migration. Mechanistic study shows that overexpression of TBK1 promoted the phosphorylation of Akt, whereas knockdown of TBK1 reverses this action. Taken together, our data suggest that TBK1 modulates the malignant behaviors of bladder cancer cell via Akt signaling, revealing new insights in discovering new therapy target for bladder cancer.

Keywords: bladder cancer, TBK1, Akt signaling