[1042] Epithelial-Mesenchymal Transition (EMT) in Non Endometrioid Endometrial Carcinomas

N Montserrat, D Llobet, C Pons, J Pena, A Gallardo, M Cuatrecasas, X Dolcet, X Matias-Guiu, J Prat. Hospital de la Santa Creu i Sant Pau. Autonomous University of Barcelona, Barcelona, Spain; Hospital Arnau de Vilanova, University of Lleida, Lleida, Spain

Background: Epithelial-mesenchymal transition (EMT) is involved in the development of invasion and metastasis. Snail is a transcription factor that regulates the EMT program. We investigated the expression of EMT genes and proteins in non-endometrioid endometrial carcinomas (NEEC).
Design: The tumors investigated included: 7 serous, 3 clear cell, 2 undifferentiated, and 6 mixed endometrial carcinomas. Tissue-arrays for immunohistochemical analysis of Snail, Twist, E-cadherin N-cadherin, and vimentin were done. Expression of Snail, Twist, E-cadherin, Zeb-1, and HMGA2 was evaluated by real time RT-PCR. Ishikawa cells (IK) overexpressing a constitutive BRAF mutation (V600) were obtained and EMT markers were then analyzed. Clinicopathologic data were collected.
Results: Expression of Snail, Twist, Zeb-1, vimentin, and HMGA2, was found to be increased in NEEC compared with normal tissue (p<0.05). An inverse correlation between Snail, Twist and Zeb-1 upregulation and E-cadherin downregulation (p<0.05) was found. IK cells overexpressing BRAFV600 showed an induced mesenchymal phenotype with alterations in EMT proteins.
Conclusions: The mRNA and protein expression of EMT markers are increased in NEEC. IK cells overexpressing BRAFV600 showed EMT features that correlate with our observations in human tumor samples.
Category: Gynecologic

Wednesday, March 11, 2009 1:00 PM

Poster Session VI # 148, Wednesday Afternoon