Clinical & Experimental Metastasis

, Volume 25, Issue 6, pp 643–655

Phenotypic plasticity of neoplastic ovarian epithelium: unique cadherin profiles in tumor progression


  • Laurie G. Hudson
    • Department of Pharmaceutical Sciences, College of PharmacyUniversity of New Mexico
  • Reema Zeineldin
    • Department of Pharmaceutical Sciences, College of PharmacyUniversity of New Mexico
    • Department of Pathology and Anatomical Sciences, School of MedicineUniversity of Missouri
Research Paper

DOI: 10.1007/s10585-008-9171-5

Cite this article as:
Hudson, L.G., Zeineldin, R. & Stack, M.S. Clin Exp Metastasis (2008) 25: 643. doi:10.1007/s10585-008-9171-5


The mesodermally derived normal ovarian surface epithelium (OSE) displays both epithelial and mesenchymal characteristics and exhibits remarkable phenotypic plasticity during post-ovulatory repair. The majority of epithelial ovarian carcinomas (EOC) are derived from the OSE and represent the most lethal of all gynecological malignancies, as most patients (∼70%) present at diagnosis with disseminated intra-abdominal metastasis. The predominant pattern of EOC metastasis involves pelvic dissemination rather than lymphatic or hematologic spread, distinguishing EOC from other solid tumors. Acquisition of the metastatic phenotype involves a complex series of interrelated cellular events leading to dissociation (shedding) and dispersal of malignant cells. A key event in this process is disruption of cell–cell contacts via modulation of intercellular junctional components. In contrast to most carcinomas that downregulate E-cadherin expression during tumor progression, a unique feature of primary well-differentiated ovarian cancers is a gain of epithelial features, characterized by an increase in expression of E-cadherin. Subsequent reacquisition of mesenchymal features is observed in more advanced tumors with concomitant loss of E-cadherin expression and/or function during progression to metastasis. The functional consequences of this remarkable phenotypic plasticity are not fully understood, but may play a role in modulation of cell survival in suspension (ascites), chemoresistance, and intraperitoneal anchoring of metastatic lesions.


Ovarian cancerEpitheliumCadherinKeratinVimentinEpithelial–mesenchymal transitionPlasticity

Copyright information

© Springer Science+Business Media B.V. 2008