MiR-582-5p Inhibits Bladder Cancer-Genesis by Suppressing TTK Expression

被引:19
|
作者
Tian, Yudong [1 ]
Guan, Yanbin [2 ]
Su, Yang [1 ]
Luo, Wenjian [1 ]
Yang, Guo [1 ]
Zhang, Yu [1 ]
机构
[1] Zhengzhou Univ, Dept Urol, Affiliated Hosp 1, 1 Longhu Zhonghuan Rd, Zhengzhou 450000, Peoples R China
[2] Henan Univ Tradit Chinese Med, Sch Pharm, Zhengzhou 450000, Henan, Peoples R China
来源
关键词
bladder cancer; miR-582-5p; TTK; proliferation; apoptosis; REGULATES CELL-PROLIFERATION; LUNG-CANCER; KINASE TTK; MICRORNA-582-5P; CONTRIBUTES; APOPTOSIS;
D O I
10.2147/CMAR.S274835
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background: Bladder cancer (BC) refers to the malignant growth found in the cells and tissues of the urinary bladder. While many studies have researched the progression of BC, scientists are yet to fully understand the mechanism of BC. This research aimed to explore the role of miR-582-5p and its target gene TTK in BC pathogenesis. Methods: The evaluation of miR-582-5p and TTK mRNA expression in BC tissues or cells was performed using qRT-PCR. TargetScan was then used to predict the binding site of miR-582-5p on TTK mRNA. Subsequently, dual-luciferase reporter and RNA pull-down assays were employed to validate the binding relationship between miR-582-5p and TTK mRNA. CCK-8, BrdU, flow cytometry, and caspase-3 activity assays were later conducted to evaluate the viability, proliferation, cell cycle, and apoptosis of BC cells. Results: Investigations revealed that miR-582-5p was downregulated in BC tissues and cells. Meanwhile, miR-582-5p inhibited the viability and proliferation of BC cells while stimulating the apoptosis and cycle arrest of the cells. TTK, the target gene of miR-582-5p, was later found to be over-expressed in BC tissues and cells. TTK, however, was observed to exhibit an opposite effect on miR-582-5p. Simply put, it stimulated BC cell malignant phenotypes, and this stimulation could be directly reversed by miR-582-5p. Conclusion: This research confirmed that miR-582-5p could restrain bladder carcinogenesis by inhibiting TTK expression.
引用
收藏
页码:11933 / 11944
页数:12
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