Loss of CCAAT/enhancer binding protein delta promotes chromosomal instability.

Abstract

The transcription factor CCAAT/enhancer binding protein delta (Cebpd, also known as C/EBPdelta, CRP3, CELF, NF-IL6beta) 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.

• Authors: A-Mei Huang, Cristina Montagna, Shikha Sharan, Yajun Ni, Thomas Ried, Esta Sterneck
• Journal: Oncogene (Oncogene) Vol. 23 Issue 8 Pg. 1549-57 (Feb 26 2004) ISSN: 0950-9232 [Print] England
• PMID: 14716301 (Publication Type: Journal Article)

Chemical References

• Biomarkers
• CCAAT-Enhancer-Binding Proteins
• Cebpd protein, mouse
• Transcription Factors
• CCAAT-Enhancer-Binding Protein-delta

Topics

• Animals
• Biomarkers (analysis)
• CCAAT-Enhancer-Binding Protein-delta
• CCAAT-Enhancer-Binding Proteins (deficiency, genetics, physiology)
• Cell Division
• Chromosomal Instability
• Fibroblasts (cytology)
• Gene Expression Regulation
• Karyotyping
• Mice (embryology)
• Mice, Knockout (embryology)
• NIH 3T3 Cells
• Transcription Factors (deficiency, genetics, physiology)