gms | German Medical Science

27th German Cancer Congress Berlin 2006

German Cancer Society (Frankfurt/M.)

22. - 26.03.2006, Berlin

Proliferation and Cell-Cell Fusion of Endometrial Carcinoma are induced by the Human Endogenous Retroviral Syncytin and regulated by TGF-β

Meeting Abstract

  • corresponding author presenting/speaker Reiner Strick - Universitätsklinikum, Erlangen, Deutschland
  • Sven Ackermann - Universitätsklinikum, Erlangen
  • Manuela Langbein - Universitätsklinikum, Erlangen
  • Matthias W Beckmann - Universitätsklinikum, Erlangen
  • Pamela L Strissel - Universitätsklinikum, Erlangen

27. Deutscher Krebskongress. Berlin, 22.-26.03.2006. Düsseldorf, Köln: German Medical Science; 2006. DocPO365

The electronic version of this article is the complete one and can be found online at:

Published: March 20, 2006

© 2006 Strick et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Endometrial carcinoma (EnCa) of endometrioid type mainly represents a steroid hormone driven tumor progression initiated from pre-stages. Due to the cell biological resemblance between the process of fetal blastocyst invasion and steroid hormone controlled growth into the maternal Endometrium and the development of tumor cells, we asked the question, if the human endogenous retroviral (HERV)-W envelope gene, Syncytin, could be involved in the cell biology and tumorigenesis of endometrioid EnCa and its pre-clinical stages.

Syncytin was found significantly increased at the mRNA and protein levels in EnCa and their pre-stages, as compared to patient matched control Endometrium. Steroid hormone treatment of EnCa induced Syncytin due to a new estrogen receptor response element in the LTR of HERV-W resulting in increased proliferation. Activation of the cAMP signalling pathway also resulted in Syncytin up-regulation, but induced EnCa cell-cell fusions similar to placental syncytiotrophoblasts. Multinucleated syncytial cells were identified in paraffin sections of endometrioid EnCa samples. Steroid hormone induced cell proliferation and EnCa cell-cell fusions were blocked using Syncytin siRNA, establishing Syncytin as main contributor to these rather opposite cell outcomes. Steroid hormone inducible TGF-β1/ β3 abrogated cell-cell fusion leading to cell proliferation, whereas TGF-β1 / β3 neutralization induced cell-cell fusions, revealing TGF-β1 / β3 as key regulators. The steroid hormone induction of Syncytin leading to increased cell proliferation contributes to the etiology of endometrioid EnCa tumor progression, which could also be essential for other steroid hormone driven tumors. Although Syncytin is a known placental bona fide gene involved in cell-cell fusions leading to syncytiotrophoblasts, Syncytin also mediates EnCa cell-cell fusions upon cAMP stimulation. The identification of Syncytin as the key mediator of cell-cell fusions in EnCa tumor biology could help to unravel the functional role of cell fusions occurring in development and in other so called syncytial cell tumors.