| Literature DB >> 26282171 |
Roxane M Pommier1, Johann Gout1, David F Vincent1, Lindsay B Alcaraz1, Nicolas Chuvin1, Vanessa Arfi1, Sylvie Martel1, Bastien Kaniewski1, Guillaume Devailly1, Geneviève Fourel1, Pascal Bernard2, Caroline Moyret-Lalle3, Stéphane Ansieau1, Alain Puisieux3, Ulrich Valcourt1, Stéphanie Sentis3, Laurent Bartholin4.
Abstract
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. ©2015 American Association for Cancer Research.Entities:
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Year: 2015 PMID： 26282171 DOI： 10.1158/0008-5472.CAN-14-3426
Source DB: PubMed Journal: Cancer Res ISSN： 0008-5472 Impact factor: 12.701