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.
Wednesday, March 11, 2009 1:00 PM
Poster Session VI # 148, Wednesday Afternoon