Unknown

Dataset Information

0

TBK1 Promote Bladder Cancer Cell Proliferation and Migration via Akt Signaling.


ABSTRACT: 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.

SUBMITTER: Chen W 

PROVIDER: S-EPMC5556653 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

altmetric image

Publications

TBK1 Promote Bladder Cancer Cell Proliferation and Migration via Akt Signaling.

Chen Wei W   Luo Kewang K   Ke Zhiyi Z   Kuai Bin B   He Shiyang S   Jiang Wei W   Huang Weiren W   Cai Zhiming Z  

Journal of Cancer 20170703 10


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 atte  ...[more]

Similar Datasets

| S-EPMC6667728 | biostudies-literature
| S-EPMC5446711 | biostudies-literature
| S-EPMC8379827 | biostudies-literature
| S-EPMC7488983 | biostudies-literature
| S-EPMC5696239 | biostudies-literature