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.
Original language | English (US) |
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Pages (from-to) | 1549-1557 |
Number of pages | 9 |
Journal | Oncogene |
Volume | 23 |
Issue number | 8 |
DOIs | |
State | Published - Feb 26 2004 |
Externally published | Yes |
Keywords
- C/EBP
- Chromosomal rearrangements
- Genomic instability
- Mouse embryo fibroblast
- Tumor suppressor
ASJC Scopus subject areas
- Molecular Biology
- Genetics
- Cancer Research