ArticleExperimental and therapeutic medicine2025
Aurora kinase A promotes epithelial‑mesenchymal transition by regulating P130 and P107 molecules in thyroid cancer cells.
Article in Experimental and therapeutic medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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