Aurora kinase A promotes epithelial-mesenchymal transition by regulating P130 and P107 molecules in thyroid cancer cells

被引:0
|
作者
Yang, Liyun [1 ,2 ]
Gao, Yuhuan [3 ]
Lu, Jing [2 ]
Wu, Geping [1 ]
机构
[1] Soochow Univ, Zhangjiagang Hosp, Dept Otolaryngol, 68 Jiyang West Rd, Suzhou 215600, Jiangsu, Peoples R China
[2] Gongli Hosp Shanghai Pudong New Area, Dept Otolaryngol, Shanghai 200135, Peoples R China
[3] Yangzhou Univ, Med Coll, Yangzhou 225009, Jiangsu, Peoples R China
关键词
thyroid cancer; epithelial mesenchymal transition; Aurora kinase A; cell cycle; signal transduction;
D O I
10.3892/etm.2025.12843
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The mortality associated with thyroid cancer (THCA) has been increasing due to distant metastasis, yet the precise mechanisms remain unclear. The present study examined the role of Aurora kinase A (AURKA) in THCA cells. Reducing AURKA expression led to decreased cell proliferation and inhibited the transition of BHT101 and BCPAP cells from the G0 phase to active division. Interestingly, decreasing AURKA expression also enhanced the cells' ability to move, migrate and invade. It was found that AURKA regulates key molecules involved in cell proliferation. Specifically, reducing AURKA expression increased the levels of P130 and E2F4, while decreasing the level of P107. Furthermore, upregulating AURKA promoted epithelial-mesenchymal transition (EMT), whereas downregulating AURKA had the opposite effect. Blocking the focal adhesion kinase signaling pathway impaired the movement, migration and invasion capabilities of THCA cells, underscoring its crucial role in metastasis. In conclusion, AURKA promotes EMT by regulating P130 and P107, thereby facilitating the metastasis of THCA.
引用
收藏
页数:13
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