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TIF1γ Suppresses Tumor Progression by Regulating Mitotic Checkpoints and Chromosomal Stability. 2015
Roxane M Pommier, and
Johann Gout, and
David F Vincent, and
Lindsay B Alcaraz, and
Nicolas Chuvin, and
Vanessa Arfi, and
Sylvie Martel, and
Bastien Kaniewski, and
Guillaume Devailly, and
Geneviève Fourel, and
Pascal Bernard, and
Caroline Moyret-Lalle, and
Stéphane Ansieau, and
Alain Puisieux, and
Ulrich Valcourt, and
Stéphanie Sentis, and
Laurent Bartholin
Inserm U1052, Centre de Recherche en Cancérologie de Lyon, Lyon, France. CNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, Lyon, France. Université de Lyon, Lyon, France. Université Lyon 1, Lyon, France. Centre Léon Bérard, Lyon, France.
The transcription accessory factor TIF1γ/TRIM33/RFG7/PTC7/Ectodermin functions as a tumor suppressor that promotes development and cellular differentiation. However, its precise function in cancer has been elusive. In the present study, we report that TIF1γ inactivation causes cells to accumulate chromosomal defects, a hallmark of cancer, due to attenuations in the spindle assembly checkpoint and the post-mitotic checkpoint. TIF1γ deficiency also caused a loss of contact growth inhibition and increased anchorage-independent growth in vitro and in vivo. Clinically, reduced TIF1γ expression in human tumors correlated with an increased rate of genomic rearrangements. Overall, our work indicates that TIF1γ exerts its tumor-suppressive functions in part by promoting chromosomal stability.
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