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Carcinogenesis Advance Access originally published online on April 29, 2007
Carcinogenesis 2007 28(10):2069-2073; doi:10.1093/carcin/bgm107
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Fat-specific FUS-DDIT3-transgenic mice establish PPAR{gamma} inactivation is required to liposarcoma development

Pedro Antonio Pérez-Mancera{dagger}, Carolina Vicente-Dueñas{dagger}, Inés González-Herrero, Manuel Sánchez-Martín1, Teresa Flores-Corral2 and Isidro Sánchez-García*

Experimental Therapeutics and Translational Oncology Program, Instituto de Biología Molecular y Celular del Cáncer, Consejo Superior de Investigaciones Científicas/Universidad de Salamanca, Campus Unamuno, 37007 Salamanca, Spain
1 Department of Medicine
2 Servicio de Anatomía Patológica, Universidad de Salamanca, Campus Unamuno, 37007 Salamanca, Spain

* To whom correspondence should be addressed. Tel: +34 923 238403; Fax: +34 923 294813; Email: isg{at}usal.es

FUS-DDIT3 is a chimeric oncogene generated by the most common chromosomal translocation t(12;16)(q13;p11) associated to liposarcomas. The application of transgenic methods and the use of primary mesenchymal progenitor cells to the study of this sarcoma-associated FUS-DDIT3 gene fusion have provided insights into their in vivo functions and suggested mechanisms by which lineage selection may be achieved. These studies indicate that FUS-DDIT3 contributes to differentiation arrest acting at a point in the adipocyte differentiation process after induction of peroxisome proliferator-activated receptor {gamma} (PPAR{gamma}) expression. To test this idea within a living mouse, we generated mice expressing FUS-DDIT3 within aP2-positive cells, because aP2 is a downstream target of PPAR{gamma} expressed at the immature adipocyte stage. Here, we report that FUS-DDIT3 expression was successfully induced at the aP2 stage of differentiation both in vivo and in vitro. aP2-FUS-DDIT3 mice do not develop liposarcomas and exhibit an increase in white adipose tissue size. Consistent with in vivo data, mouse embryonic fibroblasts (MEFs) obtained from aP2-FUS-DDIT3 mice not only were capable of terminal differentiation but also showed an increased capacity for adipogenesis in vitro compared with wild-type MEFs. Taken together, this study provides genetic evidence that the presence of FUS-DDIT3 in an aP2-positive cell is not enough to cause liposarcoma development and establishes that PPAR{gamma} inactivation is required for liposarcoma development.

Abbreviations: BAT, brown adipose tissue; MEF, mouse embryonic fibroblast; PBS, phosphate-buffered saline; PPAR{gamma}, peroxisome proliferator-activated receptor {gamma}; WAT, white adipose tissue

{dagger} These authors contributed equally to this work.

Received March 2, 2007; revised March 27, 2007; accepted April 24, 2007.


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