医学分子生物学杂志 ›› 2024, Vol. 21 ›› Issue (6): 581-585.doi: 10.3870/j.issn.1672-8009.2024.06.013

• 论著 • 上一篇    下一篇

非编码 RNA TUG1 通过调控 P38 MAPK 信号通路影响膀胱癌的体外转移活性 #br#

  

  1. 保定市第二医院1泌尿外科,2急诊科 河北省保定市, 071000
  • 出版日期:2024-11-30 发布日期:2024-12-09
  • 基金资助:
    保定市科技计划项目 (No. 2341ZF030)

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

摘要: 目的 探究长链非编码 RNA 牛磺酸上调基因 1 ( long non-coding RNA taurine-upregulated gene 1,lnc TUG1) 对膀胱癌细胞转移活性的影响以及相关机制方法 收集保定市第二医院治疗的膀胱尿路上皮癌患者的组织样本, 通过实时荧光定量 PCR 检测 lnc TUG1 P38 丝裂原活化蛋白激酶 (P38 mitogen-activated protein kinases, P38 MAPK) 的表达水平将人膀胱癌细胞系 5637 细胞分为 3 : si NC 、 si TUG1 si P38 si NC、 si TUG1 si P38 质粒转染至对应的实验组, 并通过细胞集落形成实验、 Transwell 实验流式细胞术和蛋白质印迹实验检测细胞的生长能力侵袭能力凋亡率以及 P38 MAPK 的表达水平结果 与癌旁组织比较, 癌组织 lnc TUG1 表达水平增加, P38 MAPK 的表达水平降低si NC 组比较, si TUG1 组膀胱癌细胞的集落形成数量侵袭数量显著降低凋亡率显著升高; si P38 组膀胱癌细胞的集落形成数量侵袭显著增加凋亡率显著降低si NC 组比较, si TUG1 组膀胱癌细胞的 P38 MAPK 蛋白表达明显上调结论 抑制非编码 RNA TUG1 表达能够抑制膀胱癌细胞的集落形成能力和侵袭能力, 并能促进膀胱癌细胞凋亡此外, 非编码 RNA TUG1 对膀胱癌细胞的这一作用与抑制 P38 MAPK 有关

关键词: lnc TUG1, 膀胱癌, 转移, P38 MAPK, 侵袭, 凋亡

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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