Related Experiment Video
Updated: May 17, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Aurora kinase A promotes epithelial‑mesenchymal transition by regulating P130 and P107 molecules in thyroid cancer
Liyun Yang1,2, Yuhuan Gao3, Jing Lu2
1Department of Otolaryngology, Zhangjiagang Hospital Affiliated to Soochow University, Suzhou, Jiangsu 215600, P.R. China.
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.
Insights
Aurora kinase A (AURKA) drives thyroid cancer (THCA) metastasis by promoting cell movement and epithelial-mesenchymal transition (EMT). Inhibiting AURKA reduces cancer cell proliferation and invasion, offering potential therapeutic targets.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Thyroid cancer (THCA) mortality is rising due to distant metastasis.
- The underlying mechanisms driving THCA metastasis remain largely unknown.
Purpose of the Study:
- To investigate the role of Aurora kinase A (AURKA) in THCA cell proliferation and metastasis.
- To elucidate the molecular pathways regulated by AURKA in THCA progression.
Main Methods:
- AURKA expression was modulated in THCA cell lines (BHT101, BCPAP).
- Cell proliferation, cell cycle transition, and migratory/invasive capabilities were assessed.
- Key regulatory molecules (P130, E2F4, P107) and signaling pathways (focal adhesion kinase) were analyzed.
- Epithelial-mesenchymal transition (EMT) was evaluated in response to AURKA modulation.
Main Results:
- Reduced AURKA expression decreased THCA cell proliferation and inhibited G0 to active division transition.
- Lowering AURKA levels enhanced cell motility, migration, and invasion.
- AURKA regulates cell proliferation molecules, increasing P130 and E2F4 while decreasing P107.
- AURKA upregulation promoted EMT; downregulation reversed this effect.
- Focal adhesion kinase pathway inhibition impaired THCA cell movement and invasion.
Conclusions:
- AURKA promotes THCA metastasis by driving EMT.
- AURKA regulates P130 and P107, influencing EMT and facilitating cancer spread.
- Targeting AURKA may offer a therapeutic strategy against THCA metastasis.
Related Concept Videos
PI3K/mTOR/AKT Signaling Pathway
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Mitogens and the Cell Cycle
MAPK Signaling Cascades
Abnormal Proliferation
Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

