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极光激酶A通过调节甲状腺癌细胞中的P130和P107分子来促进上皮-间质转化。

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

作者信息

Yang Liyun, Gao Yuhuan, Lu Jing, Wu Geping

机构信息

Department of Otolaryngology, Zhangjiagang Hospital Affiliated to Soochow University, Suzhou, Jiangsu 215600, P.R. China.

Department of Otolaryngology, Gongli Hospital of Shanghai Pudong New Area, Shanghai 200135, P.R. China.

出版信息

Exp Ther Med. 2025 Mar 12;29(5):93. doi: 10.3892/etm.2025.12843. eCollection 2025 May.

DOI:10.3892/etm.2025.12843
PMID:40162054
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11947869/
Abstract

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.

摘要

由于远处转移,甲状腺癌(THCA)相关的死亡率一直在上升,但其确切机制仍不清楚。本研究探讨了极光激酶A(AURKA)在THCA细胞中的作用。降低AURKA表达导致细胞增殖减少,并抑制BHT101和BCPAP细胞从G0期向活跃分裂的转变。有趣的是,降低AURKA表达还增强了细胞的移动、迁移和侵袭能力。研究发现,AURKA调节参与细胞增殖的关键分子。具体而言,降低AURKA表达会增加P130和E2F4的水平,同时降低P107的水平。此外,上调AURKA促进上皮-间质转化(EMT),而下调AURKA则产生相反的效果。阻断粘着斑激酶信号通路会损害THCA细胞的移动、迁移和侵袭能力,突显了其在转移中的关键作用。总之,AURKA通过调节P130和P107促进EMT,从而促进THCA的转移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9829/11947869/2d5c9292c0a7/etm-29-05-12843-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9829/11947869/6bde16aede20/etm-29-05-12843-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9829/11947869/971360fb4505/etm-29-05-12843-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9829/11947869/860627c88a3f/etm-29-05-12843-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9829/11947869/05a661d520ce/etm-29-05-12843-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9829/11947869/be9fab20e40c/etm-29-05-12843-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9829/11947869/c2a8d9fbd3d1/etm-29-05-12843-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9829/11947869/2d5c9292c0a7/etm-29-05-12843-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9829/11947869/6bde16aede20/etm-29-05-12843-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9829/11947869/971360fb4505/etm-29-05-12843-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9829/11947869/860627c88a3f/etm-29-05-12843-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9829/11947869/05a661d520ce/etm-29-05-12843-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9829/11947869/be9fab20e40c/etm-29-05-12843-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9829/11947869/c2a8d9fbd3d1/etm-29-05-12843-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9829/11947869/2d5c9292c0a7/etm-29-05-12843-g06.jpg

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本文引用的文献

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Elife. 2024 Sep 11;12:RP89486. doi: 10.7554/eLife.89486.
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Lymph node metastasis related gene BICC1 promotes tumor progression by promoting EMT and immune infiltration in pancreatic cancer.淋巴结转移相关基因 BICC1 通过促进 EMT 和免疫浸润促进胰腺癌的肿瘤进展。
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Erratum: LncRNA THUMPD3-AS1 promotes invasion and EMT in gastric cancer by regulating the miR-1297/BCAT1 pathway.
勘误:长链非编码RNA THUMPD3-AS1通过调控miR-1297/BCAT1通路促进胃癌侵袭和上皮间质转化。
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Role of Mir-452-5p Overexpression in Epithelial-Mesenchymal Transition (EMT) in Early-stage Colorectal Cancer.Mir-452-5p 过表达在早期结直肠癌上皮间质转化(EMT)中的作用。
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