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Updated: Jan 28, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Annexin A2 Silencing Inhibits Proliferation and Epithelial-to-mesenchymal Transition through p53-Dependent Pathway in
Minhua Wu1, Yanqin Sun2, Feipeng Xu3
1Department of Histology and Embryology, Guangdong Medical University, Zhanjiang 524023, Guangdong, China.
Abstract:
Annexin A2 has been involved in cancer cell adhesion, invasion and metastasis. However, the exact function and mechanism of Annexin A2 in tumor progression of NSCLCs have not been elucidated. In this study, we showed that Annexin A2 was evidently overexpressed in human NSCLCs cell lines and NSCLCs tissues. Clinicopathologic analysis showed that Annexin A2 expression was significantly correlated with clinical stage, and lymph node metastasis. Kaplan-Meier analysis revealed that patients with high Annexin A2 expression had poorer overall survival rates than those with low Annexin A2 expression. Moreover, we found that knockdown of Annexin A2 significantly suppressed cell proliferation and invasion of NSCLCs cells. Mechanistically, our studies showed that knockdown of Annexin A2 increased the expression of p53, which in turn, induced cell cycle G2 arrest and inhibited epithelial-to-mesenchymal transition (EMT). Taken together, these data suggest that Annexin A2 plays an important role in NSCLCs progression, which could serve as a potential prognosis marker and a novel therapeutic target for NSCLCs.
Insights
Annexin A2 is overexpressed in non-small cell lung cancers (NSCLCs), promoting tumor progression and metastasis. Reducing Annexin A2 inhibits NSCLC growth and invasion, suggesting it as a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Annexin A2 is implicated in cancer cell adhesion, invasion, and metastasis.
- The precise role and mechanism of Annexin A2 in non-small cell lung cancer (NSCLC) progression remain unclear.
Purpose of the Study:
- To investigate the function and mechanism of Annexin A2 in NSCLC tumor progression.
- To evaluate Annexin A2 as a potential prognostic marker and therapeutic target for NSCLC.
Main Methods:
- Quantitative analysis of Annexin A2 expression in NSCLC cell lines and tissues.
- Correlation analysis between Annexin A2 expression and clinicopathological features.
- Kaplan-Meier survival analysis.
- In vitro knockdown experiments of Annexin A2.
- Western blot analysis to assess p53 expression, cell cycle, and epithelial-to-mesenchymal transition (EMT) markers.
Main Results:
- Annexin A2 was significantly overexpressed in NSCLC tissues and cell lines.
- High Annexin A2 expression correlated with advanced clinical stage and lymph node metastasis.
- Patients with high Annexin A2 expression exhibited poorer overall survival.
- Knockdown of Annexin A2 suppressed NSCLC cell proliferation and invasion.
- Annexin A2 knockdown led to increased p53 expression, G2 cell cycle arrest, and inhibition of EMT.
Conclusions:
- Annexin A2 plays a crucial role in NSCLC progression.
- Annexin A2 serves as a potential prognostic biomarker for NSCLC.
- Annexin A2 represents a novel therapeutic target for NSCLC treatment.
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