Related Experiment Video
Updated: Mar 23, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Aurora kinase A induces papillary thyroid cancer lymph node metastasis by promoting cofilin-1 activity
Yusufu Maimaiti1, Tan Jie1, Zhou Jing1
1Department of Breast and Thyroid Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Abstract:
Aurora-A (Aur-A), a member of the serine/threonine Aurora kinase family, plays an important role in ensuring genetic stability during cell division. Previous studies indicated that Aur-A possesses oncogenic activity and may be a valuable therapeutic target in cancer therapy. However, the role of Aur-A in the most common thyroid cancer, papillary thyroid cancer (PTC), remains largely unknown. In patients with PTC, cancer cell migration and invasion account for most of the metastasis, recurrence, and cancer-related deaths. Cofilin-1 (CFL-1) is the most important effector of actin polymerization and depolymerization, determining the direction of cell migration. Here, we assessed the correlation between Aur-A and CFL-1 in PTC with lymph node metastasis. Tissue microarray data showed that simultaneous overexpression of Aur-A and CFL-1 correlated with lymph node metastasis in thyroid cancer tissue. Inhibition of Aur-A suppressed thyroid cancer cell migration in vitro and decreased lymph node metastasis in nude mice. Importantly, Aur-A increased the non-phosphorylated, active form of CFL-1 in TPC-1 cells, thus promoting cancer cell migration and thyroid cancer lymph node metastasis. Our findings indicate that the combination of Aur-A and CFL-1 may be useful as a molecular prediction model for lymph node metastasis in thyroid cancer and raise the possibility of targeting Aur-A and CFL-1 for more effective treatment of thyroid cancer.
Insights
Aurora-A (Aur-A) and Cofilin-1 (CFL-1) are overexpressed in papillary thyroid cancer, promoting lymph node metastasis. Targeting both Aur-A and CFL-1 may offer a new therapeutic strategy for thyroid cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Aurora-A (Aur-A) is a serine/threonine kinase crucial for cell division and possesses oncogenic properties.
- Papillary thyroid cancer (PTC) metastasis, driven by cell migration and invasion, is a major cause of mortality.
- The role of Aur-A in PTC and its association with metastasis were previously unclear.
Purpose of the Study:
- To investigate the correlation between Aur-A and Cofilin-1 (CFL-1) in PTC with lymph node metastasis.
- To determine the functional role of Aur-A in thyroid cancer cell migration and metastasis.
- To explore the potential of Aur-A and CFL-1 as therapeutic targets for PTC.
Main Methods:
- Tissue microarray analysis of thyroid cancer tissues to assess Aur-A and CFL-1 expression.
- In vitro assays to evaluate the effect of Aur-A inhibition on thyroid cancer cell migration.
- In vivo studies using nude mice to assess the impact of Aur-A inhibition on lymph node metastasis.
- Western blot analysis to examine CFL-1 phosphorylation status in response to Aur-A modulation.
Main Results:
- Simultaneous overexpression of Aur-A and CFL-1 was significantly correlated with lymph node metastasis in PTC.
- Inhibition of Aur-A reduced thyroid cancer cell migration in vitro and decreased lymph node metastasis in vivo.
- Aur-A was found to increase the active, non-phosphorylated form of CFL-1, thereby enhancing cell migration and metastasis.
Conclusions:
- The combined expression of Aur-A and CFL-1 serves as a potential molecular predictor for lymph node metastasis in thyroid cancer.
- Targeting Aur-A and CFL-1 concurrently presents a promising therapeutic strategy for improving outcomes in thyroid cancer patients.
- This study elucidates a novel mechanism by which Aur-A promotes thyroid cancer metastasis via CFL-1 activation.
Related Concept Videos
PI3K/mTOR/AKT Signaling Pathway
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
mTOR Signaling and Cancer Progression
Anaphase Promoting Complex
MAPK Signaling Cascades
M-Cdk Drives Transition Into Mitosis
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...

