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  • Original Paper
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Loss of CCAAT/enhancer binding protein δ promotes chromosomal instability

Abstract

The transcription factor CCAAT/enhancer binding protein δ (Cebpd, also known as C/EBPδ, CRP3, CELF, NF-IL6β) is implicated in diverse cellular functions such as the acute phase response, adipocyte differentiation, learning and memory, and mammary epithelial cell growth control. Here, we report that lack of Cebpd causes genomic instability and centrosome amplifications in primary embryonic fibroblasts derived from 129S1 mice. Upon spontaneous immortalization, Cebpd-deficient fibroblasts acquire transformed features such as impaired contact inhibition and reduced serum dependence. These data identify a novel role for Cebpd in the maintenance of chromosomal stability and suggest a potential tumor suppressor function in vivo.

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Acknowledgements

We thank Mary Beth Hilton, Barbara Shankle and Lori Warg for expert technical assistance, and Danny Wangsa for help with mouse SKY kits preparation. We thank David Ron, J.L. Salisbury, Claudio Schneider, Richard Janssen and Debbie Morrison for valuable reagents and advice; Karen Vousden's laboratory for generous support with resources and expert advice; Karen Vousden, Shyam Sharan and Lino Tessarollo for critical reading of the manuscript.

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Correspondence to Esta Sterneck.

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Huang, AM., Montagna, C., Sharan, S. et al. Loss of CCAAT/enhancer binding protein δ promotes chromosomal instability. Oncogene 23, 1549–1557 (2004). https://doi.org/10.1038/sj.onc.1207285

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