Related Experiment Video For SNAI2
Updated: Jan 30, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
Immunohistochemical analysis of the epithelial to mesenchymal transition in uterine carcinosarcoma
Mitsumasa Osakabe1, Daisuke Fukagawa1, Chie Sato1
1Department of Molecular Diagnostic Pathology, School of Medicine, Iwate Medical University, Morioka, Japan.
Objective:
Uterine carcinosarcoma (UCS) is a highly aggressive neoplasm that is composed of an intricate admixture of carcinomatous and sarcomatous elements. The relationship between UCS and the epithelial to mesenchymal transition (EMT) has been reported. In this study, we examined how expression of E-cadherin was associated with the expression of EMT-related proteins in UCS.
Methods:
UCS samples were histologically divided into three components: carcinomatous, transitional, and sarcomatous regions. Next, we examined the expression of E-cadherin and EMT-related proteins, including SNAI2, ZEB1, and TWIST1, in each component of the UCS using immunohistochemistry. The expression score was determined by combining the staining intensity and staining area of the target cells.
Results:
The expression score of E-cadherin was significantly lower in transitional and sarcomatous components than in the carcinomatous component. In addition, a significant difference in the low expression score of E-cadherin between transitional and sarcomatous components (transitional > sarcomatous components) was found. There were significant differences between the expression scores of ZEB1 in the three components (sarcomatous > transitional > carcinomatous components). However, no difference in the expression of TWIST1 between the components was found. Conversely, the expression level of SNAI2 was higher in sarcomatous or transitional components than in the carcinomatous component. However, a significant difference between the transitional and sarcomatous components was not detected.
Conclusion:
These results suggest that the EMT plays an essential role in the pathogenesis of UCS.
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