Epithelial-mesenchymal interconversions and the regulatory function of the ZEB family during the development and progression of ovarian cancer.

Abstract

This study assessed the role of epithelial-mesenchymal interconversions and the regulatory functions of the ZEB family during the development and progression of ovarian cancer. E-cadherin, vimentin, ZEB1 and ZEB2 were analyzed using immunohistochemistry in a series of ovarian tissues that included normal tissue, benign tumors, borderline tumors, malignant tumors and metastatic lesions. The correlation between E-cadherin and ZEB was analyzed. We also analyzed the association between the expression of the four factors and clinicopathological features in ovarian cancer. The results revealed that E-cadherin was weakly positive in normal ovarian epithelium. Cytoplasmic E-cadherin was significantly increased in benign tumors (P<0.01) and further increased in borderline tumors and ovarian cancers. However, cytoplasmic E-cadherin was markedly reduced in metastatic lesions (P<0.01). Membranous E-cadherin was increased in benign tumors, but decreased progressively in borderline, malignant and metastatic tumor tissues (P<0.05). The expression profile of vimentin was opposite to that of membranous E-cadherin. Membranous E-cadherin was negatively correlated with ZEB2 expression (r=-0.514). Additionally, cytoplasmic E-cadherin, ZEB1 and ZEB2 were associated with the FIGO stage of ovarian cancer. ZEB1 was also correlated with ascitic fluid volume. Our results suggest that epithelial-mesenchymal interconversions are dynamically regulated during the development and progression of ovarian tumors. ZEB2, but not ZEB1, may regulate the expression of membranous E-cadherin during these processes.