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.

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.

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