Expression of E-Cadherin in Normal, Benign, and Malignant Tissues of Female Genital Organs

Abstract

The expression of human E-cadherin in normal tissues and in benign and malignant tumors of female genital organs was examined immunohistochemically with a monoclonal antibody, HECD-1, specific for human E-cadherin. The normal tissues included the ovary, fallopian tube, uterine endometrium, uterine cervix, and vagina. E-cadherin was detected clearly in the cell-to-cell boundaries of both normal glandular and squamous epithelia obtained from those tissues. The tumor tissues consisted of 9 ovarian, 7 endometrial, and 4 cervical adenocarcinomas, 12 squamous cell carcinomas of the cervix, including 3 cervical intraepithelial neoplasms, and 5 mesenchymal tumors. E-cadherin also was detected in the cell-to-cell borders of all the epithelial tumors tested, with some reactivity in the cytoplasm of malignant cells, whereas mesenchymal tumors showed no expression. It is noteworthy that poorly differentiated areas of both the adenocarcinomas and squamous cell carcinomas showed less expression of E-cadherin. No difference in the expression of E-cadherin between the primary and metastatic lesions was detected in 10 sets of malignant tumors. E-cadherin may be an important factor among a variety of biologic events that occur during the process of metastasis. However, further studies are needed to clarify this.

E-cadherin promotes proliferation of human ovarian cancer cells in vitro via activating MEK/ERK pathway

“…Consistently, the up-regulation of E-cadherin expression has been considered as a new epithelial feature for OSE at the early stages of neoplastic transformation [23] . The E-cadherin expression is diminished at later stages of tumor progression as cells de-differentiate and acquire mesenchymal properties associated with a more aggressive phenotype [23][24][25] .…”

“…The E-cadherin expression is diminished at later stages of tumor progression as cells de-differentiate and acquire mesenchymal properties associated with a more aggressive phenotype [23][24][25] . Furthermore, a growing volume of data indicate that cell-cell adhesion mediated by E-cadherin is involved in the suppression of anoikis and maintenance of cellular survival in both epithelial cells, such as normal enterocytes [26] , oral squamous carcinoma cells [12] and nonepithelia such as Ewing tumor cells [27] .…”

Chromosome alterations and E-cadherin gene mutations in human lobular breast cancer

“…Its expression was reduced in several types of human carcinomas (Shimoyama et al, 1991;Bussemakers et al, 1992;Inoue et al, 1992;Umbas et al, 1992). Mutations of the E-cadherin gene have been identified in human tumours and tumour cell lines (Becker et al, 1993(Becker et al, , 1994Kanai et al, 1994;Oda et al, 1994;Risinger et al, 1994;Berx et al, 1995aBerx et al, , 1996.…”

Induction of FGF receptor 2-IIIb expression and response to its ligands in epithelial ovarian cancer

“…This increased commitment to a complex epithelial phenotype is re¯ected in molecular terms by induction of E-cadherin (Inoue et al, 1992;Veatch et al, 1994;MainesBandiera and Auersperg, 1997;Sundfeldt et al, 1997;Davies et al, 1998) and CA125 (Klug et al, 1984;Bast et al, 1995) expression in the majority of EOCs. Moreover, primary cultures of OSE from women with family histories of EOC also show phenotypes indicative of an increased commitment to an epithelial phenotype, including retention of cytokeratin expression, lower expression of type III collagen, lack of secretion of extracellular matrix and induction of CA125 expression (Dyck et al, 1996).…”