Journal of Medical Molecular Biology ›› 2024, Vol. 21 ›› Issue (6): 581-585.doi: 10.3870/j.issn.1672-8009.2024.06.013

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Non Coding RNA TUG1 Affects the in vitro Metastatic Activity of Bladder Cancer Cells by Regulating P38 MAPK Signaling Pathway #br#

  

  1. 1Department of Urology,2Department of Emergency, Baoding Second Hospital, Baoding, Hebei, 071000, China
  • Online:2024-11-30 Published:2024-12-09

Abstract: Objective To investigate the effect of Long non-coding RNA taurine-upregulatedgene 1 (lnc TUG1) on the metastasis of bladder cancer cells and the related mechanism. Methods Tissue samples were collected from patients with bladder urothelial carcinoma treated in BaodingSecond Hospital, and the expression levels of lnc TUG1 and P38 mitogen-activated protein kinases(P38 MAPK) in tissues were detected by real-time fluorescence quantitative PCR. Human bladdercancer cell line 5637 cells were divided into three groups: siNC group, si TUG1 group and si P38 group. The siNC, si TUG1 and si P38 plasmids were transfected into the corresponding experimentalgroups, and the cell growth ability, invasion ability, apoptosis rate and the expression level of P38 MAPK were detected by cell colony formation assay, Transwell assay, flow cytometry and Westernblotting. Results The expression level of TUG1 was increased, while the expression level of P38MAPK was decreased in the cancer tissues when compared with those in the cancer tissues. The number of colony formation and invasion of bladder cancer cells in the si TUG1 group was significantly decreased, the apoptosis rate was significantly increased, and the expression level of P38MAPK protein in the si TUG1 group was significantly up-regulated when compared with those in thesi NC group. However, the number of colony formation and invasion of bladder cancer cells in the si P38 group were significantly increased, and the apoptosis rate was significantly decreased whencompared with those in the siNC group. Conclusion Inhibition of lnc TUG1expression can inhibit the colony formation ability and invasion ability of bladder cancer cells, and promote the apoptosis of bladder cancer cells, and the potential mechanism might be associated with the inhibition of P38 MAPK.

Key words: lnc TUG1, bladder cancer, metastasis, P38 MAPK, invasion, apoptosis

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