NLK Promotes the Proliferation, Migration, Invasion, and EMT of Bladder Cancer Cells by Regulating Paxillin

Jianjun Lu; Qin Yu; Lixiong Chen

Authors

Jianjun Lu Department of Urology，the Thired People's Hospital, 311115 Hangzhou, Zhejiang, China Author
Qin Yu Department of Urology，Beilun District People's Hospital, 315000 Ningbo, Zhejiang, China Author
Lixiong Chen Department of Urology，the Thired People's Hospital, 311115 Hangzhou, Zhejiang, China Author

Keywords:

Bladder cancer, NLK, otolithiasis, Paxillin, EMT

Abstract

Objective: This research was intended to exploring the effect and mechanism of Nemo like kinase (NLK) and paxillin on proliferation, migration, invasion, and epithelial mesenchymal transition (EMT) of bladder cancer cells, and providing theoretical basis for basic research, clinical prevention and treatment of bladder cancer. Methods: The expression of NLK in bladder cancer tissue was analyzed by bioinformatics analysis. The proliferation, migration and invasion of bladder cancer cells were detected by EdU staining assay, clone formation assay, and transwell assay. RNA pull down assay was used to detect the interaction between NLK and paxillin in bladder cancer cells. Western blot assay was performed to measure the expressions of NLK, p-paxillin, and EMT-related proteins in bladder cancer cells. Results: NLK and p-paxillin were highly expressed in bladder cancer. NLK interacted with paxillin. NLK silencing inhibited the proliferation, migration, invasion, EMT, and p-paxillin expression of bladder cancer cells. Paxillin overexpression reversed the effect of NLK silencing on proliferation, migration, invasion, EMT, and p-paxillin expression in bladder cancer cells. Conclusion: NLK promotes the proliferation, migration, invasion and EMT of bladder cancer cells by regulating paxillin, providing theoretical basis for basic research, clinical prevention and treatment of bladder cancer.

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