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Updated: Dec 18, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
TOP2A Promotes Cell Migration, Invasion and Epithelial-Mesenchymal Transition in Cervical Cancer via Activating the
Bi Wang1,2, Yaping Shen3, Yin Zou4
1Key Laboratory of Endemic and Ethnic Diseases, Ministry of Education, Guizhou Medical University, Guiyang, Guizhou, People's Republic of China.
Topoisomerase IIA (TOP2A) is highly expressed in cervical cancer, promoting cell migration, invasion, and epithelial-mesenchymal transition (EMT) by activating the PI3K/AKT pathway.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Topoisomerase IIA (TOP2A) exhibits high expression in cervical cancer.
- The specific role of TOP2A in cervical cancer progression, particularly in migration, invasion, and EMT, is not well understood.
Purpose of the Study:
- To investigate the effect of TOP2A on cervical cancer cell migration, invasion, and epithelial-mesenchymal transition (EMT).
- To elucidate the underlying molecular mechanism by which TOP2A influences these processes, focusing on the PI3K/AKT signaling pathway.
Main Methods:
- Western blotting to assess TOP2A expression in cervical cancer tissues and cell lines.
- Transwell assays to evaluate cell migration and invasion capabilities.
- Analysis of cell morphology and epithelial-mesenchymal transition (EMT) markers (E-cadherin, N-cadherin).
- Inhibition of PI3K/AKT signaling using LY294002 to determine its role in TOP2A-mediated effects.
Main Results:
- TOP2A was overexpressed in 85% of cervical cancer tissues compared to normal tissues.
- TOP2A repression in SiHa cells reduced migration, invasion, and induced an epithelial phenotype (increased E-cadherin).
- TOP2A overexpression in Hela cells enhanced migration, invasion, and EMT (decreased E-cadherin, increased N-cadherin).
- TOP2A modulates PI3K/AKT signaling, with increased p-AKT upon TOP2A overexpression and decreased p-AKT upon TOP2A silencing.
- Inhibition of PI3K/AKT signaling partially reversed TOP2A-induced promotion of migration, invasion, and EMT.
Conclusions:
- TOP2A is abnormally overexpressed in cervical cancer.
- TOP2A overexpression drives cervical cancer cell migration, invasion, and EMT.
- These effects are mediated through the activation of the PI3K/AKT signaling pathway.
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